Text2Scene: Text-driven Indoor Scene Stylization with Part-aware Details

We propose Text2Scene, a method to automatically create realistic textures for virtual scenes composed of multiple objects. Guided by a reference image and text descriptions, our pipeline adds detailed texture on labeled 3D geometries in the room such that the generated colors respect the hierarchical structure or semantic parts that are often composed of similar materials. Instead of applying flat stylization on the entire scene at a single step, we obtain weak semantic cues from geometric segmentation, which are further clarified by assigning initial colors to segmented parts. Then we add texture details for individual objects such that their projections on image space exhibit feature embedding aligned with the embedding of the input. The decomposition makes the entire pipeline tractable to a moderate amount of computation resources and memory. As our framework utilizes the existing resources of image and text embedding, it does not require dedicated datasets with high-quality textures designed by skillful artists. To the best of our knowledge, it is the first practical and scalable approach that can create detailed and realistic textures of the desired style that maintain structural context for scenes with multiple objects.Comment: Accepted to CVPR 202

Akt1-Inhibitor of DNA binding2 is essential for growth cone formation and axon growth and promotes central nervous system axon regeneration.

Mechanistic studies of axon growth during development are beneficial to the search for neuron-intrinsic regulators of axon regeneration. Here, we discovered that, in the developing neuron from rat, Akt signaling regulates axon growth and growth cone formation through phosphorylation of serine 14 (S14) on Inhibitor of DNA binding 2 (Id2). This enhances Id2 protein stability by means of escape from proteasomal degradation, and steers its localization to the growth cone, where Id2 interacts with radixin that is critical for growth cone formation. Knockdown of Id2, or abrogation of Id2 phosphorylation at S14, greatly impairs axon growth and the architecture of growth cone. Intriguingly, reinstatement of Akt/Id2 signaling after injury in mouse hippocampal slices redeemed growth promoting ability, leading to obvious axon regeneration. Our results suggest that Akt/Id2 signaling is a key module for growth cone formation and axon growth, and its augmentation plays a potential role in CNS axonal regeneration

SelecMix: Debiased Learning by Contradicting-pair Sampling

Neural networks trained with ERM (empirical risk minimization) sometimes learn unintended decision rules, in particular when their training data is biased, i.e., when training labels are strongly correlated with undesirable features. To prevent a network from learning such features, recent methods augment training data such that examples displaying spurious correlations (i.e., bias-aligned examples) become a minority, whereas the other, bias-conflicting examples become prevalent. However, these approaches are sometimes difficult to train and scale to real-world data because they rely on generative models or disentangled representations. We propose an alternative based on mixup, a popular augmentation that creates convex combinations of training examples. Our method, coined SelecMix, applies mixup to contradicting pairs of examples, defined as showing either (i) the same label but dissimilar biased features, or (ii) different labels but similar biased features. Identifying such pairs requires comparing examples with respect to unknown biased features. For this, we utilize an auxiliary contrastive model with the popular heuristic that biased features are learned preferentially during training. Experiments on standard benchmarks demonstrate the effectiveness of the method, in particular when label noise complicates the identification of bias-conflicting examples.Comment: NeurIPS 202

Chaperone-E3 Ligase Complex HSP70-CHIP Mediates Ubiquitination of Ribosomal Protein S3

In addition to its role in ribosome biogenesis, ribosomal protein S3 (RPS3), a component of the 40S ribosomal subunit, has been suggested to possess several extraribosomal functions, including an apoptotic function. In this study, we demonstrated that in the mouse brain, the protein levels of RPS3 were altered by the degree of nutritional starvation and correlated with neuronal apoptosis. After endurable short-term starvation, the apoptotic function of RPS3 was suppressed by Akt activation and Akt-mediated T70 phosphorylation, whereas after prolonged starvation, the protein levels of RPS3 notably increased, and abundant neuronal death occurred. These events coincided with ubiquitination and subsequent degradation of RPS3, controlled by HSP70 and the cochaperone E3 ligase: carboxy terminus of heat shock protein 70-interacting protein (CHIP). Thus, our study points to an extraribosomal role of RPS3 in balancing neuronal survival or death depending on the degree of starvation through CHIP-mediated polyubiquitination and degradation

The roles of multifunctional protein ErbB3 binding protein 1 (EBP1) isoforms from development to disease

Cell biology: deciphering differences between “sibling” proteins A pair of proteins that originate from a common gene exert strikingly different effects on embryonic development as well as tumor growth and progression. RNA transcripts generated from the PA2G4 gene can undergo enzymatic processing to yield two different protein products, p42 EB1 and p48 EB1. These proteins differ by the presence or absence of 54 amino acids at one end, and Jee-Yin Ahn at the Sungkyunkwan University School of Medicine, Suwon, South Korea, and colleagues have reviewed current insights into the functional consequences of this difference. The two proteins bind to distinct sets of molecular partners. The p48 form appears to regulate a host of genes involved in brain development, but also appears to drive cancerous growth in various tumors. In contrast, p42 is scarcer during development, and appears to inhibit tumor formation

Comparative Longitudinal Analysis of Malignant Transformation in Pleomorphic Adenoma and Recurrent Pleomorphic Adenoma

Background: Recurrence in pleomorphic adenoma (PA) has been debated as a risk factor for malignant transformation (MT). In this study, we investigated whether recurrence is a risk factor for MT, by longitudinally analyzing cases with recurrent PA (RPA), and carcinomas from PA (CXPA) or RPA (CXRPA). Methods: The study population included 24 CXPA, 24 RPA, 6 CXRPA, and 386 PA cases (study period 2010–2018). Time and event data were collected from the medical documents to identify the time–event sequences. Results: The time interval to MT in CXRPA was significant longer than that of benign recurrence (median 342.0 vs. 109.5 months). In CXRPA, the recurrence intervals were not shorter than those in RPA according to recurrence frequency. Crudely, the MT rate was 5.9% among primary cases and 20.0% among recurrent cases. However, the time-adjusted MT rates increased up to 11.4% (incubation time > 60 months) and 20.0% (>120 months) in primary cases, which were not different from recurrent cases. Conclusion: In these longitudinal analyses, we did not find any clinical evidence that recurrence facilitates MT in the background of PA. Instead, a long incubation time seems to be a key factor for MT of underlying RPA

Akt regulates neurite growth by phosphorylation-dependent inhibition of radixin proteasomal degradation

Abstract Neurite growth is controlled by a complex molecular signaling network that regulates filamentous actin (F-actin) dynamics at the growth cone. The evolutionarily conserved ezrin, radixin, and moesin family of proteins tether F-actin to the cell membrane when phosphorylated at a conserved threonine residue and modulate neurite outgrowth. Here we show that Akt binds to and phosphorylates a threonine 573 residue on radixin. Akt-mediated phosphorylation protects radixin from ubiquitin-dependent proteasomal degradation, thereby enhancing radixin protein stability, which permits proper neurite outgrowth and growth cone formation. Conversely, the inhibition of Akt kinase or disruption of Akt-dependent phosphorylation reduces the binding affinity of radixin to F-actin as well as lowers radixin protein levels, resulting in decreased neurite outgrowth and growth cone formation. Our findings suggest that Akt signaling regulates neurite outgrowth by stabilizing radixin interactions with F-actin, thus facilitating local F-actin dynamics

Human UCB-MSCs treatment upon intraventricular hemorrhage contributes to attenuate hippocampal neuron loss and circuit damage through BDNF-CREB signaling

Abstract Background Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) have been shown to prevent brain damage and improve neurocognition following intraventricular hemorrhage (IVH). However, the molecular mechanisms underlying the effects of hUCB-MSCs are still elusive. Thus, as the hippocampus is essential for learning, memory, and cognitive functions and is intimately involved in the ventricular system, making it a potential site of IVH-induced injury, we determined the molecular basis of the effects of hUCB-derived MSCs on hippocampal neurogenesis and the recovery of hippocampal neural circuits after IVH in a rodent model. Methods We inflicted severe IVH injury on postnatal day 4 (P4) in rats. After confirmation of successful induction of IVH using MRI (P5), intracerebroventricular administration of MSCs (ICV-MSC) was performed at 2 days post-injury (P6). For hippocampal synaptic determination, a rat entorhinal-hippocampus (EH) organotypic slice co-culture (OSC) was performed using day 3 post-IVH brains (P7) with or without ICV-MSCs. A similar strategy of experiments was applied to those rats receiving hUCB-MSC transfected with BDNF-Si-RNA for knockdown of BDNF or scrambled siRNA controls after IVH. The molecular mechanism of the MSCs effects on neurogenesis and the attenuation of neuron death was determined by evaluation of BDNF-TrkB-Akt-CREB signaling axis. Results We showed that treatment with hUCB-MSCs attenuated neuronal loss and promoted neurogenesis in the hippocampus, an area highly vulnerable to IVH-induced brain injury. hUCB-MSCs activate BDNF-TrkB receptor signaling, eliciting intracellular activation of Akt and/or Erk and subsequent phosphorylation of CREB, which is responsible for promoting rat BDNF transcription. In addition to the beneficial effects of neuroprotection and neurogenesis, hUCB-MSCs also contribute to the restoration of impaired synaptic circuits in the hippocampus and improve neurocognitive functions in IVH-injured neonatal rat through BDNF-TrkB-CREB signaling axis activation. Conclusions Our data suggest that hUCB-MSCs possess therapeutic potential for treating neuronal loss and neurocognitive dysfunction in IVH through the activation of intracellular TrkB-CREB signaling that is invoked by hUCB-MSC-secreted BDNF