Deciphering the population structure and genetic basis of growth traits from whole-genome resequencing of the leopard coral grouper ( Plectropomus leopardus).

The leopard coral grouper ( Plectropomus leopardus) is a species of significant economic importance. Although artificial cultivation of P. leopardus has thrived in recent decades, the advancement of selective breeding has been hindered by the lack of comprehensive population genomic data. In this study, we identified over 8.73 million single nucleotide polymorphisms (SNPs) through whole-genome resequencing of 326 individuals spanning six distinct groups. Furthermore, we categorized 226 individuals with high-coverage sequencing depth (≥14×) into eight clusters based on their genetic profiles and phylogenetic relationships. Notably, four of these clusters exhibited pronounced genetic differentiation compared with the other populations. To identify potentially advantageous loci for P. leopardus, we examined genomic regions exhibiting selective sweeps by analyzing the nucleotide diversity ( θπ) and fixation index ( F ST) in these four clusters. Using these high-coverage resequencing data, we successfully constructed the first haplotype reference panel specific to P. leopardus. This achievement holds promise for enabling high-quality, cost-effective imputation methods. Additionally, we combined low-coverage sequencing data with imputation techniques for a genome-wide association study, aiming to identify candidate SNP loci and genes associated with growth traits. A significant concentration of these genes was observed on chromosome 17, which is primarily involved in skeletal muscle and embryonic development and cell proliferation. Notably, our detailed investigation of growth-related SNPs across the eight clusters revealed that cluster 5 harbored the most promising candidate SNPs, showing potential for genetic selective breeding efforts. These findings provide a robust toolkit and valuable insights into the management of germplasm resources and genome-driven breeding initiatives targeting P. leopardus.

The role of regulated necrosis in inflammation and ocular surface diseases.

In recent decades, numerous types of regulated cell death have been identified, including pyroptosis, ferroptosis and necroptosis. Regulated necrosis is characterized by a series of amplified inflammatory responses that result in cell death. Therefore, it has been suggested to play an essential role in the pathogenesis of ocular surface diseases. The cell morphological features and molecular mechanisms of regulated necrosis are discussed in this review. Furthermore, it summarizes the role of ocular surface diseases, such as dry eye, keratitis, and cornea alkali burn, as potential disease prevention and treatment targets.

Association between poor sleep quality and an increased risk of dry eye disease in patients with obstructive sleep apnea syndrome.

Purpose: Obstructive sleep apnea (OSA) is related to an increased incidence of dry eye disease (DED). However, their exact relationship is unknown and requires further well-designed studies with advanced mechanisms detection. Patients and methods: This case-control study included 125 OSA cases and 125 age-gender-matched controls enrolled in the hospital between 1 January and 1 October 2021. OSA diagnosis and classification were performed using a polysomnography (PSG) assay. Detailed ophthalmological examinations, including the Schirmer I test, corneal staining, and ocular surface disease index (OSDI), were used to detect DED-related parameters. A comprehensive ocular surface assay was performed to measure a series of parameters, including first non-invasive first tear film break-up time (f-NIBUT), average non-invasive first tear film break-up time (av-NIBUT), tear meniscus height (TMH), and loss of meibomian gland. In addition, the Pittsburgh Sleep Quality Index (PSQI) scale was used to assess sleep quality. Results: Compared to the control, the OSA group showed an increased DED risk (P = 0.016) along with an increased PSQI score and a higher rate of poor quality sleep (P < 0.001 and P = 0.007, respectively). Stratification of OSA cases indicated that DED-related parameters were impaired in patients with severe OSA (P < 0.05). The analysis of DED-parameters-related factors showed significant correlations between OSA-related indexes and PSQI (P < 0.05). Moreover, the poor sleep quality group in the OSA cases showed worse DED-related parameters (P < 0.05), which was not observed in the control group. Conclusion: OSA, especially the severe stage OSA, was related to an increased risk of DED. Also, sleep quality was correlated with the onset of both OSA and DED, where poor sleep quality revealed a relationship between OSA and the risk of DED. Overall, our findings provided evidence for advanced management of DED and OSA in future.

Nicotinamide mononucleotide increases cell viability and restores tight junctions in high-glucose-treated human corneal epithelial cells via the SIRT1/Nrf2/HO-1 pathway.

BACKGROUND: Diabetes mellitus (DM)-related corneal epithelial dysfunction is a severe ocular disorder; however, the effects of nicotinamide mononucleotide (NMN) on high-glucose (HG)-treated human corneal epithelial cells (HCECs) remain unclear. METHODS: We conducted an in-vitro study to examine the effects of NMN treatment on HG-treated HCECs. Cell viability was measured using trypan blue stain, mitochondrial membrane potential was measured using JC-1 stain, and intracellular reactive oxygen species and apoptosis assays were conducted using flow cytometry. Transepithelial electrical resistance (TEER) and zonula occludens-1 (ZO-1) immunofluorescence for tight junction examinations were conducted. Immunoblot analyses were conducted to analyze the expression of silent information regulator-1 (SIRT1), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) of the SIRT1/Nrf2/HO-1 pathway. RESULTS: NMN increased cell viability by reducing cell damage, reducing apoptosis, increasing cell migration, and restoring tight junctions in HG-treated HCECs. By analyzing the expressions of SIRT1, Nrf2, HO-1, NMN demonstrated protective effects via the SIRT1/Nrf2/HO-1 pathway. CONCLUSIONS: NMN increases cell viability by reversing cell damage, reducing apoptosis, increasing cell migration, and restoring tight junctions in HG-treated HCECs, and these effects may be mediated by the SIRT1/Nrf2/HO-1 pathway.