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The fundamental role of cells in safeguarding the genome's integrity against DNA double‐strand breaks (DSBs) is crucial for maintaining chromatin homeostasis and the overall genomic stability. Aberrant responses to DNA damage, known as DNA damage responses (DDRs), can result in genomic instability and contribute significantly to tumorigenesis. Unraveling the intricate mechanisms underlying DDRs following severe damage holds the key to identify therapeutic targets for cancer. Chromatin lysine acylation, encompassing diverse modifications such as acetylation, lactylation, crotonylation, succinylation, malonylation, glutarylation, propionylation, and butyrylation, has been extensively studied in the context of DDRs and chromatin homeostasis. Here, we delve into the modifying enzymes and the pivotal roles of lysine acylation and their crosstalk in maintaining chromatin homeostasis and genome integrity in response to DDRs. Moreover, we offer a comprehensive perspective and overview of the latest insights, driven primarily by chromatin acylation modification and associated regulators. An overview of lysine acylation modification connections to metabolic process. The energy resources, such as glucose, fatty acids, and amino acids, are metabolized by cells to produce different types of acyl‐CoA, which function as donors for chromatin lysine acylation modification in response to DNA‐damaging stress.

Bone cements such as polymethyl methacrylate and calcium phosphates have been widely used for the reconstruction of bone. Despite their remarkable clinical success, the low degradation rate of these materials hampers a broader clinical use. Matching the degradation rate of the materials with neo bone formation remains a challenge for bone-repairing materials. Moreover, questions such as the mechanism of degradation and how the composition of the materials contribute to the degradation property remain unanswered. Therefore, the review provides an overview of currently used biodegradable bone cements such as calcium phosphates (CaP), calcium sulfates and organic-inorganic composites. The possible degradation mechanism and clinical performance of the biodegradable cements are summarized. This paper reviews up-to-date research and applications of biodegradable cements, hoping to provide researchers in the field with inspirations and references.

Severe viral pneumonia can induce rapid expansion of KRT5+ basal-like cells in small airways and alveoli; this forms a scar-like structure that persists in the injured alveoli and impedes normal alveolar epithelium regeneration. In this study, we investigated the mechanism by which viral infection induced this remodeling response. Through comparing different lung-injury models, we demonstrated that infection induced strong IFN-γ signal-stimulated dysplastic KRT5+ cell formation. Inactivation of interferon receptor 1 (Ifngr1) reduced dysplastic cell formation, ameliorated lung fibrosis, and improved lung-function recovery. Mechanistically, IFN-γ regulated dysplastic cell formation via the focal adhesion kinase (FAK)/Yes-associated protein 1 (YAP) pathway. Inhibiting FAK/Src diminished IFN-γ-induced YAP nuclear translocation and dysplastic cell formation. Inhibiting YAP during viral infection prevented dysplastic cell formation, whereas inhibiting YAP in persistent KRT5+ cells led to their conversion into distal club cells. Importantly, human dysplastic cells exhibited elevated FAK and YAP activity, and IFN-γ treatment promoted the transformation of human alveolar progenitor cells into dysplastic cells. These findings uncover the role of infection-induced inflammatory response in alveolar remodeling and may provide potential therapeutic avenues for the treatment of alveolar remodeling in patients with severe viral pneumonia.

Primary ciliary dyskinesia (PCD; MIM 244400) is a genetic disorder, and its morbidity has been previously underestimated. Mutations in ciliary proteins underlie the disease, resulting in ciliary dysfunction. DNAH10 is an inner arm dynein heavy chain that has been shown to play a critical role in the movement of sperm flagella. In the present study, we demonstrated the presence of loss-of-function mutations in the DNAH10 gene among two families affected by primary ciliary dyskinesia. Patients displayed characteristic symptoms associated with PCD, including chronic respiratory infections, productive cough, and rhinosinusitis. Additionally, a decrease in the expression of DNAH10 was confirmed in both patients. Dnah10 knockout (KO) mice exhibited phenotypic characteristics recapitulating the PCD symptoms observed in two patients. Scanning electron microscope results showed curved and defective cilia morphology in Dnah10 KO mice. Immunostaining also showed that DNAH10 was specifically expressed in the cilia cell. Ciliary structural studies highlighted that DNAH10 interacted with candidate PCD proteins, including CFAP57, DYNLL1, and CCDC73, contributing to the formation of a double-headed inner dynein arm f (IDAf) complex. Co-IP experiment confirmed that DNAH10 can interact with CFAP57, DYNLL1, and CCDC73. We then detected the reduced expression of CFAP57, DYNLL1, and CCDC73 in patient P02 and Dnah10 KO mice. Furthermore, through proteomic analysis, we demonstrated alterations in the expression of abnormal innate immune proteins, super-molecular fiber organization, and mitochondrial respiratory chains. These findings suggested that the loss of DNAH10 leads to improper assembly of the IDAf complex, resulting in ciliary dysfunction and pulmonary fibrosis as the signature manifestation. Notably, our research findings hold substantial implications for the advancement of therapeutic strategies aimed at addressing ciliopathies.

This paper investigates the existence of positive equilibrium as well as the stability of positive equilibrium and zero equilibrium in a nonlinear size-structured hierarchical population model. Under the condition that larger individuals are more competitive advantages than smaller ones, a non-zero fixed point theorem is used to show that there is at lest one positive equilibrium in the system. Moreover, we obtain the stability results of positive equilibrium and zero equilibrium by deriving characteristic equations and establishing Liapunov function. Finally, some numerical experiments are presented.

Exploring the transient dynamics of ultrafast pulses is a fascinating frontier in ultrafast science. However, measuring rapidly varying spectrotemporal and phase information remains challenging. Here, we present an extracavity spectral phase editing method for the continuous generation of on-demand pulses and the experimental reconstruction of the wavelength-resolved phase dynamics of ultrafast pulses in a fibre laser. We first tailor a coherent, chirp-free seed spectrum into one or more sets of spectral combs. By controlling their interference, we generate diverse extracavity soliton compounds, including soliton molecules (SMs) and soliton molecular complexes (SMCs). Subsequently, we experimentally execute the equivalent round-to-round phase accumulations on the SMs and SMCs to reconstruct the various transient 32-pm-resolved phase dynamics, including oscillating phase, oscillating separation, combined oscillating phase and separation, and sliding phase, respectively. The experimental results show good agreement with previously reported findings. Our study provides a technique for both generating on-demand pulses and reconstructing transient wavelength-resolved pulse phase dynamics. Reconstructing wavelength-resolved phase dynamics of ultrafast soliton compounds is challenging due to the limitations of real-time measurement techniques. The authors present a spectral phase editing method that enables both on-demand generation and high-resolution reconstruction of transient phase dynamics in soliton molecular complexes.

In this work, we study topological states in Ammann–Beenker-tiling photonic quasicrystals made of magneto-optical materials. While conventional topological states in photonic systems with crystalline symmetry are characterized by topological invariants associated with bulk Bloch bands in momentum space, photonic systems in quasicrystal geometries typically lack exact periodicity and translational symmetry. As a result, conventional topological invariants defined in momentum space for photonic crystals, such as Chern number, are not applicable for photonic quasicrystals. Instead, a topological invariant called Bott index defined in real space could be employed for characterizing the topological properties of photonic quasicrystals, which we term as topological Bott insulators. In specific, we investigate the topological properties of photonic quasicrystals made of gyromagnetic dielectric cylinders arranged in a two-dimensional Ammann–Beenker tiling quasicrystalline lattice and find that this system supports dual-band chiral topological edge states, where the topological nature of both bandgaps is unambiguously confirmed by explicit calculations of the Bott index. Our work not only provides new insights on topological states in photonic quasicrystals based on the Ammann–Beenker-tiling, the results may also offer promising potentials for robust multiband photonic devices and applications not constrained by crystalline symmetries.

Defective left–right (LR) organization involving abnormalities in cilia ultrastructure causes laterality disorders including situs inversus (SI) and heterotaxy (Htx) with the prevalence approximately 1/10,000 births. In this study, we describe two unrelated family trios with abnormal cardiac LR patterning. Through whole-exome sequencing (WES), we identified compound heterozygous mutations (c.805-1G >C; p. Ile269GlnfsTer8/c.1117dupA; p.Thr373AsnfsTer19) (c.29T>C; p.Ile10Thr/c.356A>G; p.His119Arg) of NEK3 , encoding a NIMA (never in mitosis A)-related kinase, in two affected individuals, respectively. Protein levels of NEK3 were abrogated in Patient-1 with biallelic loss-of function (LoF) NEK3 mutations that causes premature stop codon. Subsequence transcriptome analysis revealed that NNMT (nicotinamide N -methyltransferase) and SIRT2 (sirtuin2) was upregulated by NEK3 knockdown in human retinal pigment epithelial (RPE) cells in vitro, which associates α-tubulin deacetylation by western blot and immunofluorescence. Transmission electron microscopy (TEM) analysis further identified defective ciliary ultrastructure in Patient-1. Furthermore, inner ring components of nuclear pore complex (NPC) including nucleoporin (NUP)205, NUP188, and NUP155 were significantly downregulated in NEK3-silenced cells. In conclusion, we identified biallelic mutations of NEK3 predispose individual to abnormal cardiac left–right patterning via SIRT2-mediated α-tubulin deacetylation and downregulation of inner ring nucleoporins. Our study suggested that NEK3 could be a candidate gene for human ciliopathies.

Background Effective postoperative analgesia for pediatric developmental dysplasia of the hip (DDH) surgery remains a challenge. This study aimed to compare the analgesic efficacy of a combined fascia iliaca compartment block (FICB) and quadratus lumborum block (QLB) versus patient-controlled intravenous analgesia (PCIA) in pediatric patients undergoing open reduction surgery for DDH under general anesthesia. Methods This retrospective cohort study enrolled children under 16 years old undergoing DDH surgery between January 2016 and January 2024. Patients were divided into two groups based on the analgesia received: a Block group (FICB + QLB, n  = 35) and a PCIA group ( n  = 35). The primary outcome was postoperative pain assessed by the FLACC score at 1 and 24 h. Secondary outcomes included 24-hour opioid (fentanyl) consumption, frequency of rescue non-steroidal anti-inflammatory drug (NSAID) use, and parental satisfaction. Results The study included 35 patients in the PCIA group and 35 in the block group. FLACC pain scores were significantly lower in the Block group at both 1 h (median: 3 vs. 7, p  < 0.001) and 24 h postoperatively (median: 2 vs. 5, p  < 0.001). Total opioid consumption was markedly lower in the Block group (mean: 5.97 vs. 20.66 µg/kg, p  < 0.001), as was the need for rescue NSAIDs (median administrations: 2 vs. 4, p  < 0.001). Parental satisfaction was significantly higher in the Block group ( p  < 0.001). Conclusion The combination of FICB and QLB provides superior postoperative analgesia compared to PCIA alone in children undergoing DDH surgery, significantly reducing pain scores, opioid requirements, and rescue analgesic need, while leading to higher parental satisfaction. Clinical trial number Not applicable.

Primary ciliary dyskinesia (PCD) is a rare phenotypically and genetically heterogeneous disorder resulting from abnormal cilia ultrastructure and function. Few studies have reported the phenotype and genetic characteristics of PCD caused by mutations in DNAAF3. In this study, four PCD patients with DNAAF3 mutations underwent extensive clinical assessments, cilia ultrastructural and motion evaluations. All patients presented with situs inversus totalis, neonatal respiratory distress, and sinusitis; however, they did not have recurrent infections of the lower airways. The nasal nitric oxide level of these patients was markedly reduced. The respiratory cilia were found to be uniformly immotile, with their dynein arms defects. A total of 7 (5 novel) variants in DNAAF3 were identified and cosegregated in their families by Trio-based whole-exome sequencing. As the first report on DNAAF3 mutations in PCD patients in China, our study not only contributes to a deeper appreciation of the phenotypic characteristics of patients with DNAAF3 mutations but also expands the spectrum of DNAAF3 mutations and may contribute to the genetic diagnosis of and counseling for PCD.