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Background In mammals, female fertility is influenced by the result of follicular development (ovulation or atresia). Follicular atresia is a complex physiological process that results in the degeneration of oocytes from the ovary. However, the molecular mechanisms of oocyte degeneration and key protein markers of follicular atresia remain unclear. In this study, we investigated the complex transcriptional regulatory mechanisms and protein profiles in oocytes and follicular fluid in atretic follicle stages using single-cell RNA sequencing and tandem mass tag proteomics. Results First, through paired analysis of different follicle development stages, we identified 175 atresia-specific genes and eight candidate oocyte-secreted factors, including PKG1 , YTHDF2 , and MYC . Meanwhile, we also characterized unique features of the oocyte transcriptional landscape in the atretic follicle stage that displayed cell death-related transcriptional changes and mechanisms, such as autophagy ( TBK1 and IRS4 ), necroptosis ( PKR ), and apoptosis ( MARCKS ). Moreover, we identified atresia-specific genes, namely FTH1 , TF , and ACSL4 , which may participate in regulation of oocyte ferroptosis in atretic follicles through a series of mechanisms including ferritinophagy, ferritin transport, and lipid metabolism. Additionally, we uncovered 333 differentially expressed proteins that may coordinate follicular atresia and revealed key pathways, such as negative regulation of angiogenesis, metabolic pathways, and transcription and mRNA splicing, that lead to oocyte degeneration. Finally, by combining transcriptome and proteomics analyses, we identified two oocyte-secreted biomarkers, PGK1 and ANGPT2, that may be associated with follicular atresia. Conclusions In conclusion, our work offers a thorough characterization of oocyte transcription mechanism and follicular fluid protein changes in ovine atretic follicles, which offers a crucial reference for analyzing the mechanism of follicular atresia and establishing an oocyte quality assessment system in sheep. Highlights 1. Distinct transcription regulation and protein profiles exist in healthy and atretic follicles. 2. Ferroptosis-induced oocyte degeneration occurs in atretic follicles. 3. Identification of oocyte-secreted biomarkers is associated with follicular atresia.

In this study, Cu/Ni and Cu/Al multilayers, with individual layer thickness varying from 25 nm to 200 nm, and co-sputtered Cu-Ni and Cu-Al single layer films were deposited at room temperature via magnetron sputtering and further annealed from 100 °C to 300 °C. The mechanical and microstructural properties of the as-deposited and annealed samples were characterized by nanoindentation, x-ray diffraction, and scanning electron microscopy. Both multilayer systems exhibit an increase in hardness with increasing annealing temperature. However, the Cu/Ni system shows a gradual and moderate hardness increase (up to 30%) from room temperature to 300 °C, while the Cu/Al system displays a sharp hardness surge (~150%) between 125 °C and 200 °C. The co-sputtered Cu-Ni and Cu-Al samples consistently demonstrate higher hardness than their multilayered counterparts, albeit with distinctly different temperature dependence—the hardness of Cu-Ni increases with annealing temperature while Cu-Al maintains a constant high hardness throughout the entire temperature range. The distinct thermal strengthening mechanisms observed in the two metallic multilayer systems can be ascribed to the formation of solid solutions in Cu/Ni and the precipitation of intermetallic phases in Cu/Al. This study highlights the unique advantage of intermetallic strengthening in metallic multilayer systems.

Inflammation is the common pathogenesis of coronary atherosclerosis disease (CAD) and rheumatoid arthritis (RA). Although it is established that RA increases the risk of CAD, the underlining mechanism remained indefinite. This study seeks to explore the molecular mechanisms of RA linked CAD and identify potential target gene for early prediction of CAD in RA patients. The study utilized five raw datasets: GSE55235, GSE55457, GSE12021 for RA patients, and GSE42148 and GSE20680 for CAD patients. Gene Set Enrichment Analysis (GSEA) was used to investigate common signaling pathways associated with RA and CAD. Then, weighted gene co-expression network analysis (WGCNA) was performed on RA and CAD training datasets to identify gene modules related to single-sample GSEA (ssGSEA) scores. Overlapping module genes and differentially expressed genes (DEGs) were considered as co-susceptible genes for both diseases. Three hub genes were screened using a protein-protein interaction (PPI) network analysis via Cytoscape plug-ins. The signaling pathways, immune infiltration, and transcription factors associated with these hub genes were analyzed to explore the underlying mechanism connecting both diseases. Immunohistochemistry and qRT-PCR were conducted to validate the expression of the key candidate gene, PPARG, in macrophages of synovial tissue and arterial walls from RA and CAD patients. The study found that Fc-gamma receptor-mediated endocytosis is a common signaling pathway for both RA and CAD. A total of 25 genes were screened by WGCNA and DEGs, which are involved in inflammation-related ligand-receptor interactions, cytoskeleton, and endocytosis signaling pathways. The principal component analysis(PCA) and support vector machine (SVM) and receiver-operator characteristic (ROC) analysis demonstrate that 25 DEGs can effectively distinguish RA and CAD groups from normal groups. Three hub genes TUBB2A, FKBP5, and PPARG were further identified by the Cytoscape software. Both FKBP5 and PPARG were downregulated in synovial tissue of RA and upregulated in the peripheral blood of CAD patients and differential mRNAexpreesion between normal and disease groups in both diseases were validated by qRT-PCR.Association of PPARG with monocyte was demonstrated across both training and validation datasets in CAD. PPARG expression is observed in control synovial epithelial cells and foamy macrophages of arterial walls, but was decreased in synovial epithelium of RA patients. Its expression in foamy macrophages of atherosclerotic vascular walls exhibits a positive correlation (r = 0.6276, p = 0.0002) with CD68. Our findings suggest that PPARG may serve as a potentially predictive marker for CAD in RA patients, which provides new insights into the molecular mechanism underling RA linked CAD.

To evaluate the wound healing process following direct pulp capping with demineralized bone matrix (DBM) and calcium hydroxide (Ca(OH)2). Fifty 8-weeks-old SPF Wistar male rats were divided into two groups: one was the DBM treated group, and the other was the Ca(OH)2 treated group. Pulpotomy was performed on the maxillary first molar of one side of each rat, and the another side was left as the blank control. Rats were sacrificed after each observation period (1, 3, 7, 14 and 28 days) and specimen slices were made. Hematoxylin-Eosin (HE) staining was used for observing the changes of pulp tissue, and immunohistochemical staining was used for observing the expression of reparative dentinogenesis-related factors runt transcription factor 2 (Runx2), type I collagen (COL I), osteocalcin (OCN) and dentin sialoprotein (DSP). Inflammatory cell infiltration (ICI) and pulp tissue disorganization (PTD) could be observed in both the DBM and Ca(OH)2 groups at all observation periods. The DBM group showed slighter ICI on 1 and 28 days and milder PTD on 28 days, with a significant difference (P<0.05). Reparative dentin formation (RDF) could initially be observed on 14 days postoperatively, and the DBM group showed more regular and thinner RDF with significant differences on 14 and 28 days compared with the Ca(OH)2 group (P<0.05). In both groups, the expression of Runx2, COL I, DSP and OCN were positive. Generally, the expression of these four factors in the DBM group was stronger than the Ca(OH)2 group on the same observation periods. DBM had the ability of inducing odontoblast differentiation and promoting dentinogenesis. DBM could initiate physiologic wound healing in pulp and had the ability to promote reparative dentin formation. Consequently, DBM may be an acceptable alternative for direct pulp capping.

13-Hydroxyoctadecadienoic acid (13(S)-HODE) is a bioactive lipid derived from linoleic acid, it plays prominent roles in cellular processes such as lipid metabolism, oxidative stress, and apoptosis. Follicular atresia is a complex physiological process involving multiple forms of cell death. Ferroptosis, an iron-dependent form of programmed cell death, has been less studied in the context of follicular atresia. To investigate the association between ovine follicular atresia and ferroptosis, we performed transcriptomic and metabolomic analyses of healthy and atretic sheep follicles. Notably, sheep follicular granulosa cells were treated with different doses of 13(S)-HODE. Cell viability, lipid peroxidation levels, ferroptosis-related markers, and ferroptosis-related genes were measured. The metabolomic analysis identified 87 and 48 differentially expressed metabolites in healthy and atretic follicles, respectively. Functional enrichment of atretic follicle fluid highlighted pathways related to linoleic acid and purine metabolism. Transcriptomic analysis revealed 250 highly expressed genes in ovarian granulosa cells of atretic follicles. Enrichment analysis indicated that these differentially expressed genes were associated with fatty acid metabolism and ferroptosis. Integration of multi-omics data demonstrated the occurrence of ferroptosis in atretic follicles, where 13(S)-HODE drives granulosa cell ferroptosis via the linoleic acid metabolism pathway; this effect was not dose-dependent. Mechanistic studies showed that low-dose 13(S)-HODE counteracts ferroptosis by promoting glutathione peroxidase 4-mediated lipid peroxidation reduction and increasing glutathione levels. In contrast, high-dose 13(S)-HODE induces labile iron accumulation through activation of transferrin receptor and ferritin heavy chain 1, enhancing ferroptosis sensitivity in granulosa cells. These findings provide insights into the molecular mechanisms regulating follicle development and offer potential therapeutic targets for enhanced follicular development and improved reproductive outcomes.

Golgi membrane protein 1 (GOLM1) was implicated in carcinogenesis of multiple types of cancer. However, Phosphoproteome landscapes of GOLM1 overexpression in lung cancer remain largely unknown. In this study, using data from the Cancer Genome Atlas (TCGA) and phosphoproteome, we systematically evaluated the feature of GOLM1 and studied its prognostic value in non-small cell lung cancer (NSCLC). The proliferation, migration, and invasion capacities in PC9 cell with GOLM1 overexpression were determined using Trans-well system assay. Tumor engrafts was visualized in mice models and confirmed by ex vivo. An increased expression of GOLM1 had shorter overall survival (OS) in patients with NSCLC in TCGA database. GOLM1 in single gene set enrichment analysis (GSEA) related to adherent’s junction, cell cycle, and pathway in cancer. Overexpression of GOLM1 in GOLM1OE PC9 cells promoted cell proliferation, migration, and invasion. Decreased migration and invasion potential were also observed in knockdown of GOLM1 in GOLM1KD PC9 cells in migration assay. An increased expression of GOLM1 could significantly increase the growth of tumor in xenograft mice models. phosphoproteome analysis showed 239 upregulated and 331 downregulated Phosphorylated proteins in GOLM1OE PC9 cells. Overexpression of GOLM1 in GSEA was significantly related to P53 in MAPK signaling pathway. Overexpression of GOLM1enhanced the phosphorylation of P53 protein at site S315 but inhibited the formation of P53 tetramers. These results indicate that overexpression GOLM1 enhances non-small-cell carcinoma aggressiveness through inhibited the formation of P53 tetramer.

Triple-negative breast cancer shows worse outcome compared with other subtypes of breast cancer. The discovery of dysregulated microRNAs and their roles in the progression of triple-negative breast cancer provide novel strategies for the treatment of patients with triple-negative breast cancer. In this study, we identified the significant reduction of miR-133 in triple-negative breast cancer tissues and cell lines. Ectopic overexpression of miR-133 suppressed the proliferation, colony formation, and upregulated the apoptosis of triple-negative breast cancer cells. Mechanism study revealed that the YES Proto-Oncogene 1 was a target of miR-133. miR-133 bound the 3′-untranslated region of YES Proto-Oncogene 1 and decreased the level of YES Proto-Oncogene 1 in triple-negative breast cancer cells. Consistent with miR-133 downregulation, YES1 was significantly increased in triple-negative breast cancer, which was inversely correlated with the level of miR-133. Restoration of YES Proto-Oncogene 1 attenuated the inhibitory effects of miR-133 on the proliferation and colony formation of triple-negative breast cancer cells. Consistent with the decreased expression of YES Proto-Oncogene 1, overexpression of miR-133 suppressed the phosphorylation of YAP1 in triple-negative breast cancer cells. Our results provided novel evidence for the role of miR-133/YES1 axis in the development of triple-negative breast cancer, which indicated miR-133 might be a potential therapeutic strategy for triple-negative breast cancer.

Encouraging the recycling of plastic packaging materials in express delivery is a necessary step toward environmentally friendly industrial development. In this study, we present a framework for analyzing the flow of materials in express plastic packaging, from production and manufacturing to consumption and recycling. In examining the use of recycled materials in post-consumer express plastic packaging and the destination of consumer packaging waste in 2020 and 2021, we found that 44.4% (1613.6 Gg) of the studied express plastic packaging was incinerated. Additionally, approximately 1296.6 Gg of express plastic packaging flowed into rural areas. Our calculations showed that the ΔRSE in 2020 was 15.1%, and on the condition that 25% separated collection with 80% recycling, ΔRSE would be − 0.5%. Results verified that separated collection is an important step in the recycling strategy for packaging materials. Survey data from universities in Beijing indicate that currently, 26% of college students are participating in the separate collection of packaging.

In this study, gold (Au)–indium (In) intermetallic compounds (IMCs) formation for low temperature solder bonding was investigated by imbedding a gold wire into the annealing indium solder. According to available research on liquid–solid reaction of gold and indium, experiments were only conducted at an annealing temperature in the range of 200–300 °C. To investigate the feasibility of forming the Au–In IMCs at lower temperature, a low annealing temperature of 160 °C was applied in this study, which is just above the melting point of indium of 156 °C. AuIn 2 precipitates were confirmed to be predominately formed in the IMCs by X-ray diffraction. Different annealing times of 10, 40, and 120 min were applied to study the stabilization time of IMC AuIn 2 . With thermal considerations, AuIn 2 was confirmed to form with a low annealing temperature of 160 °C, and a short annealing time of 10 min. In addition, the microstructure of the cross-sections in the interfacial region of the gold wire and indium solder was investigated by scanning electron microscopy. The mechanical behavior of gold, indium, and their IMCs with different annealing times were studied by nanoindentation. Mechanical properties including reduced modulus and hardness were extracted after taking into account of the pile-up effect. Increased reduced modulus and hardness were observed with increasing annealing times, due to the strengthening of the atomic bonding in the compounds. The reduced modulus and hardness measured from nanoindentation indicate a significant strengthening of the indium solder by the AuIn 2 nanoparticles.

The development of the ovarian antral follicle is a complex, highly regulated process. Oocytes orchestrate and coordinate the development of mammalian ovarian follicles, and the rate of follicular development is governed by a developmental program intrinsic to the oocyte. Characterizing oocyte signatures during this dynamic process is critical for understanding oocyte maturation and follicular development. Although the transcriptional signature of sheep oocytes matured in vitro and preovulatory oocytes have been previously described, the transcriptional changes of oocytes in antral follicles have not. Here, we used single-cell transcriptomics (SmartSeq2) to characterize sheep oocytes from small, medium, and large antral follicles. We characterized the transcriptomic landscape of sheep oocytes during antral follicle development, identifying unique features in the transcriptional atlas, stage-specific molecular signatures, oocyte-secreted factors, and transcription factor networks. Notably, we identified the specific expression of 222 genes in the LO, 8 and 6 genes that were stage-specific in the MO and SO, respectively. We also elucidated signaling pathways in each antral follicle size that may reflect oocyte quality and in vitro maturation competency. Additionally, we discovered key biological processes that drive the transition from small to large antral follicles, revealing hub genes involved in follicle recruitment and selection. Thus, our work provides a comprehensive characterization of the single-oocyte transcriptome, filling a gap in the mapping of the molecular landscape of sheep oogenesis. We also provide key insights into the transcriptional regulation of the critical sizes of antral follicular development, which is essential for understanding how the oocyte orchestrates follicular development.