Tri-MipRF: Tri-Mip Representation for Efficient Anti-Aliasing Neural Radiance Fields

Despite the tremendous progress in neural radiance fields (NeRF), we still face a dilemma of the trade-off between quality and efficiency, e.g., MipNeRF presents fine-detailed and anti-aliased renderings but takes days for training, while Instant-ngp can accomplish the reconstruction in a few minutes but suffers from blurring or aliasing when rendering at various distances or resolutions due to ignoring the sampling area. To this end, we propose a novel Tri-Mip encoding that enables both instant reconstruction and anti-aliased high-fidelity rendering for neural radiance fields. The key is to factorize the pre-filtered 3D feature spaces in three orthogonal mipmaps. In this way, we can efficiently perform 3D area sampling by taking advantage of 2D pre-filtered feature maps, which significantly elevates the rendering quality without sacrificing efficiency. To cope with the novel Tri-Mip representation, we propose a cone-casting rendering technique to efficiently sample anti-aliased 3D features with the Tri-Mip encoding considering both pixel imaging and observing distance. Extensive experiments on both synthetic and real-world datasets demonstrate our method achieves state-of-the-art rendering quality and reconstruction speed while maintaining a compact representation that reduces 25% model size compared against Instant-ngp.Comment: Accepted to ICCV 2023 Project page: https://wbhu.github.io/projects/Tri-MipR

Population genomics uncovers global distribution, antimicrobial resistance, and virulence genes of the opportunistic pathogen <i>Klebsiella </i>aerogenes

Klebsiella aerogenes is an understudied and clinically important pathogen. We therefore investigate its population structure by genome analysis aligned with metadata. We sequence 130 non-duplicated K. aerogenes clinical isolates and identify two inter-patient transmission events. We then retrieve all publicly available K. aerogenes genomes (n = 1,026, accessed by January 1, 2023) and analyze them with our 130 genomes. We develop a core-genome multi-locus sequence-typing scheme. We find that K. aerogenes is a species complex comprising four phylogroups undergoing evolutionary divergence, likely forming three species. We delineate remarkable clonal diversity and identify three worldwide-distributed carbapenemase-encoding clonal clusters, representing high-risk lineages. We uncover that K. aerogenes has an open genome equipped by a large arsenal of antimicrobial resistance genes. We identify two genetic regions specific for K. aerogenes, encoding a type VI secretion system and flagella/chemotaxis for motility, respectively, both contributing to the virulence. These results provide much-needed insights into the population structure and pan-genomes of K. aerogenes.</p

Lack of association between polymorphisms of MASP2 and susceptibility to SARS coronavirus infection

<p>Abstract</p> <p>Background</p> <p>The pathogenesis of severe acute respiratory disease syndrome (SARS) is not fully understood. One case-control study has reported an association between susceptibility to SARS and <it>mannan-binding lectin </it>(<it>MBL</it>) in China. As the downstream protein of <it>MBL</it>, variants of the <it>MBL</it>-associated serine protease-2 (<it>MASP2</it>) gene may be associated with SARS coronavirus (SARS-CoV) infection in the same population.</p> <p>Methods</p> <p>Thirty individuals with SARS were chosen for analysis of <it>MASP2 </it>polymorphisms by means of PCR direct sequencing. Tag single nucleotide polymorphisms (tagSNPs) were chosen using pairwise tagging algorithms. The frequencies of four tag SNPs (rs12711521, rs2261695, rs2273346 and rs7548659) were ascertained in 376 SARS patients and 523 control subjects, using the Beckman SNPstream Ultra High Throughput genotyping platform.</p> <p>Results</p> <p>There is no significant association between alleles or genotypes of the <it>MASP2 </it>tagSNP and susceptibility to SARS-CoV in both Beijing and Guangzhou populations. Diplotype (rs2273346 and rs12711521)were analyzed for association with susceptibility to SARS, no statistically significant evidence of association was observed. The Beijing and Guangzhou sample groups were homogeneous regarding demographic and genetic parameters, a joined analysis also showed no statistically significant evidence of association.</p> <p>Conclusion</p> <p>Our data do not suggest a role for <it>MASP2 </it>polymorphisms in SARS susceptibility in northern and southern China.</p

H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response

The inflammatory response and apoptosis have been proved to have a crucial role in the pathogenesis of the influenza A virus (IAV). Previous studies indicated that while IAV commonly causes pancreatitis and pancreatic damage in naturally and experimentally infected animals, the molecular mechanisms of the pathogenesis of IAV infection are less reported. In the present study, we showed for the first time that both avian-like (α-2,3-linked) and human-like (α-2,6-linked) sialic acid (SA) receptors were expressed by the mouse pancreatic cancer cell line PAN02 and the human pancreatic cancer cell line PANC-1. Using growth kinetics experiments, we also showed that PAN02 and PANC-1 cells supported the productive replication of the H5N1 highly pathogenic avian influenza while exhibited the limited replication of IAV subtypes H1N1 and H7N2 in vitro. The in vivo infection of H5N1 in pancreatic cells was confirmed by the histopathological and immunohistochemical staining of pancreas tissue from mice. Other than H1N1 and H7N2, severe damage and extensive positive signals were observed in pancreas of H5N1 infected mice. All three virus subtypes induced apoptosis but also triggered the infected PAN02 and PANC-1 cells to release pro-inflammatory cytokines and chemokines including interferon (IFN)-α, IFN-β, IFN-γ, chemokine (C-C motif) ligand 2 (CCL2), tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Notably, the subtypes of H5N1 could significantly upregulate these cytokines and chemokines in both two cells when compared with H1N1 and H7N2. The present data provide further understanding of the pathogenesis of H5N1 IAV in pancreatic cells derived from humans and mammals and may also benefit the development of new treatment against H5N1 influenza virus infection

Organic NIR-II dyes with ultralong circulation persistence for image-guided delivery and therapy

Acknowledgments This work was partially supported by grants from the National Key R&D Program of China (2020YFA0908800), NSFC (82111530209, 81773674, 91959103, 81573383, 21763002), Shenzhen Science and Technology Research Grant (JCYJ20190808152019182), the Applied Basic Research Program of Wuhan Municipal Bureau of Science and Technology (2019020701011429), Hubei Province Scientific and Technical Innovation Key Project (2020BAB058), the Local Development Funds of Science and Technology Department of Tibet (XZ202102YD0033C, XZ202001YD0028C), and the Fundamental Research Funds for the Central Universities.Peer reviewedPublisher PD

Upconversion NIR-II fluorophores for mitochondria-targeted cancer imaging and photothermal therapy

Acknowledgements: The work was supported by the National Key R&D Program of China (2020YFA0908800), NSFC (81773674, 81573383), Shenzhen Science and Technology Research Grant (JCYJ20190808152019182), Hubei Province Scientific and Technical Innovation Key Project, National Natural Science Foundation of Hubei Province (2017CFA024, 2017CFB711), the Applied Basic Research Program of Wuhan Municipal Bureau of Science and Technology (2019020701011429), Tibet Autonomous Region Science and Technology Plan Project Key Project (XZ201901-GB-11), the Local Development Funds of Science and Technology Department of Tibet (XZ202001YD0028C), Project First-Class Disciplines Development Supported by Chengdu University of Traditional Chinese Medicine (CZYJC1903), Health Commission of Hubei Province Scientific Research Project (WJ2019M177, WJ2019M178), the China Scholarship Council, and the Fundamental Research Funds for the Central Universities.Peer reviewedPublisher PD

Nanodelivery of nucleic acids

Funding: This work was supported by the European Research Council (ERC) Starting Grant (ERC-StG-2019-848325 to J. Conde) and the Fundação para a Ciência e a Tecnologia FCT Grant (PTDC/BTM-MAT/4738/2020 to J. Conde). J.S. acknowledges US National Institute of Health (NIH) grants (R01CA200900, R01HL156362 and R01HL159012), the US DoD PRCRP Idea Award with Special Focus (W81XWH1910482), the Lung Cancer Discovery Award from the American Lung Association and the Innovation Discovery Grants award from the Mass General Brigham. H.L., D.Y. and X.Z. were supported by the National Key R&D Program of China (no. 2020YFA0710700), the National Natural Science Foundation of China (nos 21991132, 52003264, 52021002 and 52033010) and the Fundamental Research Funds for the Central Universities (no. WK2060000027).There is growing need for a safe, efficient, specific and non-pathogenic means for delivery of gene therapy materials. Nanomaterials for nucleic acid delivery offer an unprecedented opportunity to overcome these drawbacks; owing to their tunability with diverse physico-chemical properties, they can readily be functionalized with any type of biomolecules/moieties for selective targeting. Nucleic acid therapeutics such as antisense DNA, mRNA, small interfering RNA (siRNA) or microRNA (miRNA) have been widely explored to modulate DNA or RNA expression Strikingly, gene therapies combined with nanoscale delivery systems have broadened the therapeutic and biomedical applications of these molecules, such as bioanalysis, gene silencing, protein replacement and vaccines. Here, we overview how to design smart nucleic acid delivery methods, which provide functionality and efficacy in the layout of molecular diagnostics and therapeutic systems. It is crucial to outline some of the general design considerations of nucleic acid delivery nanoparticles, their extraordinary properties and the structure–function relationships of these nanomaterials with biological systems and diseased cells and tissues.publishersversionpublishe

HLA Polymorphism Affects Risk of de novo Mutation of dystrophin Gene and Clinical Severity of Duchenne Muscular Dystrophy in a Southern Chinese Population

Immune-mediated pathology has been thought to be an important factor contributing to Duchenne muscular dystrophy (DMD). Allele frequencies of certain HLA types are known to differ between patients with dystrophinopathies and healthy controls with low-resolution HLA gene typing data in limit reports. Using Polymerase chain reactionsequence based typing (PCR-SBT) to genotype 64 children with DMD in HLA-A, -B,-C, -DRB1, and -DQB1 locus and 503 healthy controls in HLA-A, -B, -DRB1 locus, this study aimed to investigate associations of specific HLA alleles with, and their possible roles in the development and clinical phenotypic severity of DMD. The χ2 test was used to evaluate the distribution of allele frequencies in HLA-A, -B, -DRB1 locus between the patients and healthy controls. A significantly higher frequency of HLA-B*07:05 was found in children with DMD compared to that in controls (OR = 16.2, 95%CI = 2.9–89.3, P &lt; 0.046). More importantly, significantly higher frequencies of HLA-A*29:01 (OR = 77.308, 95%CI = 6.794–879.731, P &lt; 0.0160) and HLA-B*07:05 (OR = 60.240, 95%CI = 9.637–376.535, P &lt; 2.41*10−3) was found in patients with de novo mutations (n = 14) compared to controls while no difference of HLA alleles frequency ware indicated between patients with inherited mutation and control. The result indicates that HLA alleles is associated with pathogenesis of DMD especially DMD with de novo mutation. We use Vignos scale to estimate the lower limb motor function of patients. The impact of HLA alleles on score of Vignos scale of DMD children was estimated by multiple linear regression. Our study indicates that HLA-A*02:01 may have a dampening effect on the clinical phenotypic severity of DMD, evidenced by the presence of HLA-A*02:01 being associated with lower Vignos score. Our study demonstrates that certain HLA alleles are indeed associated with the pathogenesis and clinical phenotypic severity of DMD

The Transmembrane Protein Semaphorin 6A Repels Embryonic Sympathetic Axons

Semaphorin 6A (Sema6A) (previously named Semaphorin VIa) is the originally described member of the vertebrate semaphorin class 6, a group of transmembrane semaphorins homologous to the insect semaphorin class 1. Although Sema-1a (previously named semaphorin I) has been implicated in axon guidance in insects, the function of Sema6A is currently unknown. We have expressed the extracellular domain of Sema6A in mammalian cells as either a monomeric or a dimeric fusion protein and tested for potential axon guidance effects on two populations of embryonic neurons in growth cone collapse and collagen matrix chemorepulsion assays. Sema6A was observed to induce growth cone collapse of sympathetic neurons with an EC50 of approximately 200 pM, although a 10-fold higher (EC50 of approximately 2 nM) concentration was necessary to induce growth cone collapse of dorsal root ganglion neurons. The activity of Sema6A is likely to depend on protein dimerization or oligomerization. Although Sema6A mRNA is expressed in complex patterns during embryonic development, it is strikingly absent from sympathetic ganglia. Sema6A is, however, expressed in areas avoided by sympathetic axons and in areas innervated by sympathetics, but before their arrival. Our results demonstrate that transmembrane semaphorins, like the secreted ones, can act as repulsive axon guidance cues. Our findings are consistent with a role for Sema6A in channeling sympathetic axons into the sympathetic chains and controlling the temporal sequence of sympathetic target innervation