Cardiac Hypertrophy Involves Both Myocyte Hypertrophy and Hyperplasia in Anemic Zebrafish

Background: An adult zebrafish heart possesses a high capacity of regeneration. However, it has been unclear whether and how myocyte hyperplasia contributes to cardiac remodeling in response to biomechanical stress and whether myocyte hypertrophy exists in the zebrafish. To address these questions, we characterized the zebrafish mutant tr265/tr265, whose Band 3 mutation disrupts erythrocyte formation and results in anemia. Although Band 3 does not express and function in the heart, the chronic anemia imposes a sequential biomechanical stress towards the heart. Methodology/principal findings: Hearts of the tr265/tr265 Danio rerio mutant become larger than those of the sibling by week 4 post fertilization and gradually exhibit characteristics of human cardiomyopathy, such as muscular disarray, re-activated fetal gene expression, and severe arrhythmia. At the cellular level, we found both increased individual cardiomyocyte size and increased myocyte proliferation can be detected in week 4 to week 12 tr265/tr265 fish. Interestingly, all tr265/tr265 fish that survive after week-12 have many more cardiomyocytes of smaller size than those in the sibling, suggesting that myocyte hyperplasia allows the long-term survival of these fish. We also show the cardiac hypertrophy process can be recapitulated in wild-type fish using the anemia-inducing drug phenylhydrazine (PHZ). Conclusions/significance: The anemia-induced cardiac hypertrophy models reported here are the first adult zebrafish cardiac hypertrophy models characterized. Unlike mammalian models, both cardiomyocyte hypertrophy and hyperplasia contribute to the cardiac remodeling process in these models, thus allowing the effects of cardiomyocyte hyperplasia on cardiac remodeling to be studied. However, since anemia can induce effects on the heart other than biomechanical, non-anemic zebrafish cardiac hypertrophy models shall be generated and characterized

Space advanced technology demonstration satellite

The Space Advanced Technology demonstration satellite (SATech-01), a mission for low-cost space science and new technology experiments, organized by Chinese Academy of Sciences (CAS), was successfully launched into a Sun-synchronous orbit at an altitude of similar to 500 km on July 27, 2022, from the Jiuquan Satellite Launch Centre. Serving as an experimental platform for space science exploration and the demonstration of advanced common technologies in orbit, SATech-01 is equipped with 16 experimental payloads, including the solar upper transition region imager (SUTRI), the lobster eye imager for astronomy (LEIA), the high energy burst searcher (HEBS), and a High Precision Magnetic Field Measurement System based on a CPT Magnetometer (CPT). It also incorporates an imager with freeform optics, an integrated thermal imaging sensor, and a multi-functional integrated imager, etc. This paper provides an overview of SATech-01, including a technical description of the satellite and its scientific payloads, along with their on-orbit performance

Using Zebrafish Animal Model to Study the Genetic Underpinning and Mechanism of Arrhythmogenic Cardiomyopathy

Arrhythmogenic cardiomyopathy (ACM) is largely an autosomal dominant genetic disorder manifesting fibrofatty infiltration and ventricular arrhythmia with predominantly right ventricular involvement. ACM is one of the major conditions associated with an increased risk of sudden cardiac death, most notably in young individuals and athletes. ACM has strong genetic determinants, and genetic variants in more than 25 genes have been identified to be associated with ACM, accounting for approximately 60% of ACM cases. Genetic studies of ACM in vertebrate animal models such as zebrafish (Danio rerio), which are highly amenable to large-scale genetic and drug screenings, offer unique opportunities to identify and functionally assess new genetic variants associated with ACM and to dissect the underlying molecular and cellular mechanisms at the whole-organism level. Here, we summarize key genes implicated in ACM. We discuss the use of zebrafish models, categorized according to gene manipulation approaches, such as gene knockdown, gene knock-out, transgenic overexpression, and CRISPR/Cas9-mediated knock-in, to study the genetic underpinning and mechanism of ACM. Information gained from genetic and pharmacogenomic studies in such animal models can not only increase our understanding of the pathophysiology of disease progression, but also guide disease diagnosis, prognosis, and the development of innovative therapeutic strategies

Star Identification Algorithm Based on Multi-Dimensional Features and Multi-Layered Joint Screening for Star Sensors

The algorithm for star identification is a crucial technology for determining the orientation of spacecraft using star sensors. Traditional star identification algorithms achieve matching by seeking a unique or a few optimal solutions. However, in high-noise environments, some solutions may be lost, which could result in matching failure. A new lost-in-space architecture algorithm aimed at rapid identification under high star position noise conditions by directly using star positions for final matching is proposed in this paper. The main idea of this algorithm is to construct sufficiently redundant navigation triangles, fully utilizing the physical relationships of the features and forming a screening method from high to low dimensions and from loose to strict. During identification, a multi-layer joint screening matching method is adopted to screen triangles as a whole, narrowing the range of matches quickly while retaining error tolerance. In a series of simulation experiments, this algorithm achieved identification rates of 99.51%, 99.06%, and 98.42% for 2.0 pixel star position noise, 1.0 Mv star magnitude noise, and 5 false stars, respectively. In terms of practical application, all 1000 star images taken by the star sensor in orbit have been successfully identified, and it only takes 28ms to identify each image. In addition, star images taken by consumer-grade cameras from the ground also show that the algorithm has strong robustness to star position noise, magnitude error and false star interference in more severe environments. This method provides partial algorithmic reference for non-specialized design of star sensors for low-cost, large-scale satellites in the future

Data_Sheet_1_TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell.doc

Fowl adenovirus serotype 4 (FAdV-4) is recognized as a pathogen that causes hydropericardium syndrome. Irrespective of the pathway used by the virus to invade the chicken, the pathological characteristics of the disease include degeneration and necrosis of hepatocytes, formation of intranuclear inclusions, as well as inflammatory cell infiltration. Liver dysfunction constitutes one of the critical factors leading to death. Therefore, it is vital to investigate the virus-mediated severe pathological liver damage to further understand the pathogenesis of FAdV-4. Here, proteomics, a tandem mass tag (TMT)-based approach to directly analyze protein expression, was used to determine the protein expression during FAdV-4 proliferation in leghorn male hepatoma (LMH) cells. We identified 177 differentially expressed proteins associated with various biological processes and pathways. The functional enrichment analysis revealed that FAdV-4 could downregulate some signaling pathways in LMH cells, including NOD-like receptor signaling, RIG-I-like receptor signaling, NF-κB signaling, TNF signaling pathway, and Notch signaling, FoxO signaling, PI3K-Akt signaling, and autophagy. The results of proteomics screening suggested an association between FAdV-4 infection and Notch signaling in LMH in vitro, indicating that Notch signaling regulated the expression of inflammatory cytokines and interferons but not viral replication in LMH cells. These data contributed to the understanding of the immunopathogenesis and inflammopathogenesis of FAdV-4 infection and also provided valuable information for the further analysis of the molecular mechanisms underlying viral pathogenesis.</p

Table_2_TMT-based quantitative proteomics analysis reveals the role of Notch signaling in FAdV-4-infected LMH cell.XLSX

Fowl adenovirus serotype 4 (FAdV-4) is recognized as a pathogen that causes hydropericardium syndrome. Irrespective of the pathway used by the virus to invade the chicken, the pathological characteristics of the disease include degeneration and necrosis of hepatocytes, formation of intranuclear inclusions, as well as inflammatory cell infiltration. Liver dysfunction constitutes one of the critical factors leading to death. Therefore, it is vital to investigate the virus-mediated severe pathological liver damage to further understand the pathogenesis of FAdV-4. Here, proteomics, a tandem mass tag (TMT)-based approach to directly analyze protein expression, was used to determine the protein expression during FAdV-4 proliferation in leghorn male hepatoma (LMH) cells. We identified 177 differentially expressed proteins associated with various biological processes and pathways. The functional enrichment analysis revealed that FAdV-4 could downregulate some signaling pathways in LMH cells, including NOD-like receptor signaling, RIG-I-like receptor signaling, NF-κB signaling, TNF signaling pathway, and Notch signaling, FoxO signaling, PI3K-Akt signaling, and autophagy. The results of proteomics screening suggested an association between FAdV-4 infection and Notch signaling in LMH in vitro, indicating that Notch signaling regulated the expression of inflammatory cytokines and interferons but not viral replication in LMH cells. These data contributed to the understanding of the immunopathogenesis and inflammopathogenesis of FAdV-4 infection and also provided valuable information for the further analysis of the molecular mechanisms underlying viral pathogenesis.</p