Laplacian Projection Based Global Physical Prior Smoke Reconstruction

We present a novel framework for reconstructing fluid dynamics in real-life scenarios. Our approach leverages sparse view images and incorporates physical priors across long series of frames, resulting in reconstructed fluids with enhanced physical consistency. Unlike previous methods, we utilize a differentiable fluid simulator (DFS) and a differentiable renderer (DR) to exploit global physical priors, reducing reconstruction errors without the need for manual regularization coefficients. We introduce divergence-free Laplacian eigenfunctions (div-free LE) as velocity bases, improving computational efficiency and memory usage. By employing gradient-related strategies, we achieve better convergence and superior results. Extensive experiments demonstrate the effectiveness of our method, showcasing improved reconstruction quality and computational efficiency compared to existing approaches. We validate our approach using both synthetic and real data, highlighting its practical potential

Inhibition of Adaptive Vγ2Vδ2(+) T-Cell Responses during Active Mycobacterial Coinfection of Simian Immunodeficiency Virus SIVmac-Infected Monkeys

Adaptive immune responses of γδ T cells during active mycobacterial coinfection of human immunodeficiency virus-infected humans have not been studied. Macaques infected with the simian immunodeficiency virus (SIV) SIVmac were employed to determine the extent to which a coincident AIDS virus infection might compromise immune responses of mycobacterium-specific Vγ2Vδ2(+) T cells during active mycobacterial infection. Control SIVmac-negative macaques developed primary and recall expansions of phosphoantigen-specific Vγ2Vδ2(+) T cells after Mycobacterium bovis BCG infection and BCG reinfection, respectively. In contrast, SIVmac-infected macaques did not exhibit sound primary and recall expansions of Vγ2Vδ2(+) T cells in the blood and pulmonary alveoli following BCG infection and reinfection. The absence of adaptive Vγ2Vδ2(+) T-cell responses was associated with profound CD4(+) T-cell deficiency and subsequent development of SIVmac-related tuberculosis-like disease in the coinfected monkeys. Consistently, Vγ2Vδ2(+) T cells from coinfected monkeys displayed a reduced capacity to expand in vitro following stimulation with phosphoantigen. The reduced ability of Vγ2Vδ2(+) peripheral blood lymphocytes (PBL) to expand could be restored to some extent by coculture of these cells with CD4(+) T cells purified from PBL of SIV-negative monkeys. Furthermore, naïve monkeys inoculated simultaneously with SIVmac and BCG were unable to sustain expansion of Vγ2Vδ2(+) T cells at the time that the coinfected monkeys developed lymphoid depletion and a fatal tuberculosis-like disease. Nevertheless, no deletion in Vδ2 T-cell receptor repertoire was identified in SIVmac-BCG-coinfected macaques, implicating an SIVmac-induced down-regulation rather than a clonal exhaustion of these cells. Thus, an SIVmac-induced compromise of the adaptive Vγ2Vδ2(+) T-cell responses may contribute to the immunopathogenesis of the SIV-related tuberculosis-like disease in macaques

Regulation of p53 in the red-eared slider (Trachemys scripta elegans) in response to salinity stress

The freshwater red-eared slider (Trachemys scripta elegans) is found not only in freshwater but also in coastal saline habitats. Hyperosmotic salinity can induce cell damage. p53, regarded as the guardian of the genome, is very important and versatile in response to the change of environment. In this study, the role of p53 in T. s. elegans under environmental salinity change will be explored. The results indicated that amino acid sequence of p53 showed high similarity to p53 of other species. In addition, the expression of p53 showed differences in various tissues under normal condition. Under salinity stress, the mRNA levels of p53 in the liver increased significantly at 48 h with 15‰ group (15 practical salinity units-exposed group). In the heart, p53 mRNA levels increased at 6 h in 5‰ (5 practical salinity units) and 15‰ groups. Furthermore, the changes of p21 mRNA expression levels in liver and heart were similar to p53, while cyclin D1, cyclin-dependent kinase4 (CDK4) and cyclin-dependent kinase6 (CDK6) showed opposite changes to p53. Moreover, Bax and caspase 3 mRNA expression levels were similar to p53, respectively, while Bcl-2 showed opposite changes. The positive cells of apoptosis were found in the liver of 15‰ at 48 h and 30 d of chronic stress. Taken together, these results indicated that the T. s. elegans may protect itself by regulating cell cycle progression and apoptosis of damaged cells under salinity stress, which played an important role for T. s. elegans in salinity adaptation