Genomes shed light on the evolution of Begonia, a mega‐diverse genus

Clarifying the evolutionary processes underlying species diversification and adaptation is a key focus of evolutionary biology. Begonia (Begoniaceae) is one of the most species-rich angiosperm genera with ~2,000 species, most of which are shade-adapted. Here, we present chromosome-scale genome assemblies for four species of Begonia (B. loranthoides, B. masoniana, B. darthvaderiana, and B. peltatifolia), and whole genome shot-gun data for an additional 74 Begonia representatives to investigate lineage evolution and shade adaptation of the genus. The four genome assemblies range in size from 331.75 Mb (B. peltatifolia) to 799.83 Mb (B. masoniana), and harbor 22,059 - 23,444 protein-coding genes. Synteny analysis revealed a lineage specific whole-genome duplication (WGD) that occurred just before the diversification of the Begonia. Functional enrichment of gene families retained after WGD highlight the significance of modified carbohydrate metabolism and photosynthesis possibly linked to shade-adaptation in the genus, which is further supported by expansions of gene families involved in light perception and harvesting. Phylogenomic reconstructions and genomics studies indicate that genomic introgression has also played a role in the evolution of Begonia. Overall, this study provides valuable genomic resources for Begonia and suggests potential drivers underlying the diversity and adaptive evolution of this mega-diverse clade

Research on Cleaning Mechanism of Anti-Erosion Coating Based on Thermal and Force Effects of Laser Shock

TiN coating plays a positive role in improving the abrasion resistance and impact resistance of aero-engines in sand and dust environments. However, little research has been done on the laser cleaning of TiN coatings that failed on aircraft engines. In this paper, TiN coatings are deposited on Ti6Al4V alloys by magnetic filtered cathodic vacuum arc (MFCVA). The TiN coating was laser cleaned with different parameters. By analyzing coating morphology, surface composition and sample profile, the research reveals the morphological change of the TiN coating after cleaning and the laser cleaning mechanism. The results show that for TiN–Ti6Al4V structure, when the laser average power density is 2.54 × 103 W/cm2, the cleaning mechanism of the coating is thermal expansion; The laser average power density is increased to 5.08 × 103 W/cm2, the cleaning mechanism is thermal expansion, accompanied by the thermal melting of the substrate, a small amount of molten substrate overflows from the crack. When the laser average power density is 5.08 × 103 W/cm2 and the number of cleanings doubles, the cleaning direction is perpendicular to each other, the cleaning mechanism is thermal expansion and thermal melting, both the substrate and the coating are melted, and the cleaning is obviously effective

Myeloid Trem2 Dynamically Regulates the Induction and Resolution of Hepatic Ischemia-Reperfusion Injury Inflammation

Trem2, a transmembrane protein that is simultaneously expressed in both bone marrow-derived and embryonic-derived liver-resident macrophages, plays a complex role in liver inflammation. The unique role of myeloid Trem2 in hepatic ischemia-reperfusion (IR) injury is not precisely understood. Our study showed that in the early stage of inflammation induction after IR, Deletion of myeloid Trem2 inhibited the induction of iNOS, MCP-1, and CXCL1/2, alleviated the accumulation of neutrophils and mitochondrial damage, and simultaneously decreased ROS formation. However, when inflammatory monocyte-macrophages gradually evolved into CD11bhiLy6Clow pro-resolution macrophages through a phenotypic switch, the story of Trem2 took a turn. Myeloid Trem2 in pro-resolution macrophages promotes phagocytosis of IR-accumulated apoptotic cells by controlling Rac1-related actin polymerization, thereby actively promoting the resolution of inflammation. This effect may be exercised to regulate the Cox2/PGE2 axis by Trem2, alone or synergistically with MerTK/Arg1. Importantly, when myeloid Trem2 was over-expressed, the phenotypic transition of monocytes from a pro-inflammatory to a resolution type was accelerated, whereas knockdown of myeloid Trem2 resulted in delayed upregulation of CX3CR1. Collectively, our findings suggest that myeloid Trem2 is involved in the cascade of IR inflammation in a two-sided capacity, with complex and heterogeneous roles at different stages, not only contributing to our understanding of sterile inflammatory immunity but also to better explore the regulatory strategies and intrinsic requirements of targeting Trem2 in the event of sterile liver injury

Causal associations between sleep traits and four cardiac diseases: a Mendelian randomization study

Abstract Aims Previous studies investigated the associations between sleep traits and cardiac diseases, but the evidence for the causal inferences was unclear. This study aimed to explore the causal relationship between sleep and cardiac diseases by virtue of Mendelian randomization (MR). Methods and results Summary‐level data for exposure variables (sleep duration, chronotype, and insomnia) and outcome variables (ischaemic heart disease, atrial fibrillation, myocardial infarction, and heart failure) were derived from UK Biobank. Data from the FinnGen consortium was used as a robustness check. In MR analysis, the inverse variance weighted (IVW) method was applied to infer causality between exposure and outcome. MR‐Egger regression was used to identify pleiotropy, and MR‐PRESSO outlier test was used to remove the pleiotropy of the genetic instruments. Based on UK Biobank, MR analysis suggested that sleep duration was weakly associated with atrial fibrillation (OR = 0.9999, 95% CI: 0.9998–0.9999) and ischaemic heart disease (OR = 0.9997, 95% CI: 0.9995–0.9998). Insomnia was associated with ischaemic heart disease (OR = 1.0117, 95% CI: 1.0051–1.0183) and myocardial infarction (OR = 1.0049, 95% CI: 1.0019–1.0079). No associations were found between chronotype and cardiac diseases (P > 0.05). We did not find pleiotropy except for insomnia with ischaemic heart disease and myocardial infarction using MR‐Egger regression, and MR‐PRESSO analysis consistent with IVW. Finally, we obtained the same direction as with UK Biobank using the FinnGen data. Conclusions Sleep duration and insomnia might be the potential causal risk factors of cardiac diseases. As the OR was small, these associations are probably not clinically relevant. Further validation studies are needed

Additional file 1: Figure S1. of Depletion of histone demethylase KDM5B inhibits cell proliferation of hepatocellular carcinoma by regulation of cell cycle checkpoint proteins p15 and p27

Knockdown of KDM5B has no obvious effect on apoptosis and senescence of HCC cells. (A) FACS assays was performed to detect the difference in apoptotic cells between Hep-3B cells with or without KDM5B knockdown. (B) Senescence-associated (SA) β-galactosidase (SA-β-gal) analysis was performed to detect the difference in apoptotic cells between Hep-3B cells with or without KDM5B knockdown. The data were presented as the mean ± SD (n = 3), NS, not significant, **P < 0.01, and *** P < 0.001. (DOCX 656 kb

Interorgan communication in neurogenic heterotopic ossification: the role of brain-derived extracellular vesicles

Abstract Brain-derived extracellular vesicles participate in interorgan communication after traumatic brain injury by transporting pathogens to initiate secondary injury. Inflammasome-related proteins encapsulated in brain-derived extracellular vesicles can cross the blood‒brain barrier to reach distal tissues. These proteins initiate inflammatory dysfunction, such as neurogenic heterotopic ossification. This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies. Accordingly, a rat model of neurogenic heterotopic ossification induced by combined traumatic brain injury and achillotenotomy was developed to address these two issues. Histological examination of the injured tendon revealed the coexistence of ectopic calcification and fibroblast pyroptosis. The relationships among brain-derived extracellular vesicles, fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo. The present work highlights the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offers a potential strategy for preventing neurogenic heterotopic ossification after traumatic brain injury. Brain-derived extracellular vesicles (BEVs) are released after traumatic brain injury. These BEVs contain pathogens and participate in interorgan communication to initiate secondary injury in distal tissues. After achillotenotomy, the phagocytosis of BEVs by fibroblasts induces pyroptosis, which is a highly inflammatory form of lytic programmed cell death, in the injured tendon. Fibroblast pyroptosis leads to an increase in calcium and phosphorus concentrations and creates a microenvironment that promotes osteogenesis. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk suppressed fibroblast pyroptosis and effectively prevented the onset of heterotopic ossification after neuronal injury. The use of a pyroptosis inhibitor represents a potential strategy for the treatment of neurogenic heterotopic ossification