36 research outputs found

    IC3D: Image-Conditioned 3D Diffusion for Shape Generation

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    In the last years, Denoising Diffusion Probabilistic Models (DDPMs) obtained state-of-the-art results in many generative tasks, outperforming GANs and other classes of generative models. In particular, they reached impressive results in various image generation sub-tasks, among which conditional generation tasks such as text-guided image synthesis. Given the success of DDPMs in 2D generation, they have more recently been applied to 3D shape generation, outperforming previous approaches and reaching state-of-the-art results. However, 3D data pose additional challenges, such as the choice of the 3D representation, which impacts design choices and model efficiency. While reaching state-of-the-art results in generation quality, existing 3D DDPM works make little or no use of guidance, mainly being unconditional or class-conditional. In this paper, we present IC3D, the first Image-Conditioned 3D Diffusion model that generates 3D shapes by image guidance. It is also the first 3D DDPM model that adopts voxels as a 3D representation. To guide our DDPM, we present and leverage CISP (Contrastive Image-Shape Pre-training), a model jointly embedding images and shapes by contrastive pre-training, inspired by text-to-image DDPM works. Our generative diffusion model outperforms the state-of-the-art in 3D generation quality and diversity. Furthermore, we show that our generated shapes are preferred by human evaluators to a SoTA single-view 3D reconstruction model in terms of quality and coherence to the query image by running a side-by-side human evaluation

    Synergies and Trade-Offs of National Conservation Policy and Agro-Forestry Management Over Forest Loss in Argentina During the Last Decade

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    One reason for the decline of natural forest is that many ecosystem services (ESs) are usually not priced and values were only considered provisioning services. Argentina enacted the National Law 26,331/07, which regulates protection, enrichment, restoration and management of native forests and its environmental services. The objective is to determine the ecological and sociopolitical factors that influence the dynamics of forest cover loss before and after the lawimplementation and discuss the effectiveness of conservation and forest management policies. Satellite images, national ordination, forest regions maps and other variables were combined in GIS with national databases (social, agriculture, industry) to determine the evolution of potential drivers of forest changes. The main potential drivers were: (i) population growth, (ii) road density, (iii) crops area, (iv) livestock and (v) fires. Payment of incentives by government cannot fully stop the deforestation but decrease the forest loss rate. New approaches must be considered to built-in flexibility actions according to local conditions and constraints, which are influenced by social and economic contexts. Thus, it is necessary to establish new regional policies associated with the factors linked to the loss of forest cover, in the search for sustainable management alternatives that combine economic and conservation proposals.Laboratorio de Investigaciones en MaderaConsejo Nacional de Investigaciones CientĂ­ficas y TĂ©cnicasInstituto Nacional de TecnologĂ­a Agropecuari

    Measurement of the 244^{244}Cm and 246^{246}Cm Neutron-Induced Cross Sections at the n_TOF Facility

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    The neutron capture reactions of the 244^{244}Cm and 246^{246}Cm isotopes open the path for the formation of heavier Cm isotopes and of heavier elements such as Bk and Cf in a nuclear reactor. In addition, both isotopes belong to the minor actinides with a large contribution to the decay heat and to the neutron emission in irradiated fuels proposed for the transmutation of nuclear waste and fast critical reactors. The available experimental data for both isotopes are very scarce. We measured the neutron capture cross section with isotopically enriched samples of 244^{244}Cm and 246^{246}Cm provided by JAEA. The measurement covers the range from 1 eV to 250 eV in the n_TOF Experimental Area 2 (EAR-2). In addition, a normalization measurement with the 244^{244}Cm sample was performed at Experimental Area 1 (EAR-1) with the Total Absorption Calorimeter (TAC)

    UBPY: a growth-regulated human ubiquitin isopeptidase.

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    The ubiquitin pathway has been implicated in the regulation of the abundance of proteins that control cell growth and proliferation. We have identified and characterized a novel human ubiquitin isopeptidase, UBPY, which both as a recombinant protein and upon immunoprecipitation from cell extracts is able to cleave linear or isopeptide-linked ubiquitin chains. UBPY accumulates upon growth stimulation of starved human fibroblasts, and its levels decrease in response to growth arrest induced by cell-cell contact. Inhibition of UBPY accumulation by antisense plasmid microinjection prevents fibroblasts from entering S-phase in response to serum stimulation. By increasing or decreasing the cellular abundance of UBPY or by overexpressing a catalytic site mutant, we detect substantial changes in the total pattern of protein ubiquitination, which correlate stringently with cell proliferation. Our results suggest that UBPY plays a role in regulating the overall function of the ubiquitin-proteasome pathway. Affecting the function of a specific UBP in vivo could provide novel tools for controlling mammalian cell proliferation

    Cell cycle– and cell growth–regulated proteolysis of mammalian CDC6 is dependent on APC–CDH1

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    CDC6 is conserved during evolution and is essential and limiting for the initiation of eukaryotic DNA replication. Human CDC6 activity is regulated by periodic transcription and CDK-regulated subcellular localization. Here, we show that, in addition to being absent from nonproliferating cells, CDC6 is targeted for ubiquitin-mediated proteolysis by the anaphase promoting complex (APC)/cyclosome in G(1). A combination of point mutations in the destruction box and KEN-box motifs in CDC6 stabilizes the protein in G(1) and in quiescent cells. Furthermore, APC, in association with CDH1, ubiquitinates CDC6 in vitro, and both APC and CDH1 are required and limiting for CDC6 proteolysis in vivo. Although a stable mutant of CDC6 is biologically active, overexpression of this mutant or wild-type CDC6 is not sufficient to induce multiple rounds of DNA replication in the same cell cycle. The APC–CDH1-dependent proteolysis of CDC6 in early G(1) and in quiescent cells suggests that this process is part of a mechanism that ensures the timely licensing of replication origins during G(1)

    Expression of ICAM-1 and VCAM-1 in human malignant mesothelioma

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    Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-inducible adhesion molecules which recognize ligands that are highly expressed on leukocytes. Expression of ICAM-1 and VCAM- 1 was investigated in tissue sections of 16 cases of malignant mesothelioma (seven epithelial, eight biphasic, and one sarcomatoid) using immunohistochemistry. Neoplastic cells were diffusely and intensely stained for ICAM-1 in all cases. VCAM-1 was detected in 14 of 16 cases. The percentage of VCAM-1-positive tumour cells was more than 50 per cent in eight cases and the staining was observed mainly in epithelial-like cells. VCAM-1 was rarely expressed in other malignant tumours of epithelial origin, being present in only 1 of 58 cases of carcinoma originating from different anatomical sites. At the cellular level, ICAM-1 and VCAM-1 appeared co-distributed, the staining for both being cytoplasmic with a membrane reinforcement. The regulation of VCAM-1 expression by neoplastic mesothelial cells was investigated in vitro using 14 mesothelioma cell lines. ICAM-1 was expressed by cultured cells of all mesothelioma cell lines, even in the absence of cytokines. VCAM-1 was detected in 10-50 per cent of the cells in three non-stimulated mesothelioma cell lines (mero-95, mero-96, and mero-134), and was absent or poorly expressed in the remaining 11. Exposure of a negative cell line (mero-48a) to an optimal concentration of tumour necrosis factor alpha (TNFα) or interleukin-13 (IL- 13) for 6-18 h resulted in the induction of VCAM-1 mRNA synthesis and in VCAM- 1 expression at the membrane level in 60-70 per cent of the cells. These findings are consistent with the possibility that TNFα, IL-13, or other activating signals are released in the turnout micro-environment and regulate the expression of VCAM-1 in malignant mesothelioma cells.</p

    Expression of ICAM-1 and VCAM-1 in human malignant mesothelioma

    No full text
    Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are cytokine-inducible adhesion molecules which recognize ligands that are highly expressed on leukocytes. Expression of ICAM-1 and VCAM- 1 was investigated in tissue sections of 16 cases of malignant mesothelioma (seven epithelial, eight biphasic, and one sarcomatoid) using immunohistochemistry. Neoplastic cells were diffusely and intensely stained for ICAM-1 in all cases. VCAM-1 was detected in 14 of 16 cases. The percentage of VCAM-1-positive tumour cells was more than 50 per cent in eight cases and the staining was observed mainly in epithelial-like cells. VCAM-1 was rarely expressed in other malignant tumours of epithelial origin, being present in only 1 of 58 cases of carcinoma originating from different anatomical sites. At the cellular level, ICAM-1 and VCAM-1 appeared co-distributed, the staining for both being cytoplasmic with a membrane reinforcement. The regulation of VCAM-1 expression by neoplastic mesothelial cells was investigated in vitro using 14 mesothelioma cell lines. ICAM-1 was expressed by cultured cells of all mesothelioma cell lines, even in the absence of cytokines. VCAM-1 was detected in 10-50 per cent of the cells in three non-stimulated mesothelioma cell lines (mero-95, mero-96, and mero-134), and was absent or poorly expressed in the remaining 11. Exposure of a negative cell line (mero-48a) to an optimal concentration of tumour necrosis factor alpha (TNFα) or interleukin-13 (IL- 13) for 6-18 h resulted in the induction of VCAM-1 mRNA synthesis and in VCAM- 1 expression at the membrane level in 60-70 per cent of the cells. These findings are consistent with the possibility that TNFα, IL-13, or other activating signals are released in the turnout micro-environment and regulate the expression of VCAM-1 in malignant mesothelioma cells.</p
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