Adsorption removal of mercury from flue gas by metal selenide: A review.

Mercury (Hg) pollution has been a global concern in recent decades, posing a significant threat to entire ecosystems and human health due to its cumulative toxicity, persistence, and transport in the atmosphere. The intense interaction between mercury and selenium has opened up a new field for studying mercury removal from industrial flue gas pollutants. Besides the advantages of good Hg° capture performance and low secondary pollution of the mineral selenium compounds, the most noteworthy is the relatively low regeneration temperature, allowing adsorbent regeneration with low energy consumption, thus reducing the utilization cost and enabling recovery of mercury resources. This paper reviews the recent progress of mineral selenium compounds in flue gas mercury removal, introduces in detail the different types of mineral selenium compounds studied in the field of mercury removal, reviews the adsorption performance of various mineral selenium compounds adsorbents on mercury and the influence of flue gas components, such as reaction temperature, air velocity, and other factors, and summarizes the adsorption mechanism of different fugitive forms of selenium species. Based on the current research progress, future studies should focus on the economic performance and the performance of different carriers and sizes of adsorbents for the removal of Hg0 and the correlation between the gas-particle flow characteristics and gas phase mass transfer with the performance of Hg0 removal in practical industrial applications. In addition, it remains a challenge to distinguish the oxidation and adsorption of Hg0 quantitatively.

CasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury.

Wnt/ß-catenin signaling is an attractive target for regenerative medicine. A powerful driver of stem cell activity and hence tissue regeneration, Wnt signaling can promote fibroblast proliferation and activation, leading to fibrosis, while prolonged Wnt signaling is potentially carcinogenic. Thus, to harness its therapeutic potential, the activation of Wnt signaling must be transient, reversible and tissue-specific. In the lung, Wnt signaling is essential for alveolar stem cell activity and alveolar regeneration, which is impaired in lung fibrosis. Activation of Wnt/ß-catenin signaling in lung epithelium may have anti-fibrotic effects. Here, we used intratracheal AAV6 injection to selectively deliver CasRx into lung epithelium, where it reversibly activates Wnt signaling by simultaneously degrading mRNAs encoding Axin1 and Axin2, negative regulators of Wnt/ß-catenin signaling. Interestingly, CasRx mediated Wnt activation specifically in lung epithelium not only promotes alveolar type II cell (AT2) proliferation and alveolar regeneration, but also inhibits lung fibrosis resulted from bleomycin-induced injury, relevant in both preventive and therapeutic settings. Our study offers an attractive strategy for treating pulmonary fibrosis, with general implications for regenerative medicine.

Genesis and regulation of C-terminal cyclic imides from protein damage.

C-Terminal cyclic imides are post-translational modifications (PTMs) that can arise from spontaneous intramolecular cleavage of asparagine or glutamine residues resulting in a form of irreversible protein damage. These protein damage events are recognized and removed by the E3 ligase substrate adapter cereblon (CRBN), indicating that these aging-related modifications may require cellular quality control mechanisms to prevent deleterious effects. However, the factors that determine protein or peptide susceptibility to C-terminal cyclic imide formation or their effect on protein stability have not been explored in detail. Here, we characterize the primary and secondary structures of peptides and proteins that promote intrinsic formation of C-terminal cyclic imides in comparison to deamidation, a related form of protein damage. Extrinsic effects from solution properties and stressors on the cellular proteome additionally promote C-terminal cyclic imide formation on proteins like glutathione synthetase (GSS) that are susceptible to aggregation if the protein damage products are not removed by CRBN. This systematic investigation provides insight to the regions of the proteome that are prone to these unexpectedly frequent modifications, the effects of this form of protein damage on protein stability, and the biological role of CRBN.

Novel Conductive and Redox-Active Molecularly Imprinted Polymer for Direct Quantification of Perfluorooctanoic Acid.

This study developed a novel molecularly imprinted polymer (MIP) that is both conductive and redox-active for directly quantifying perfluorooctanoic acid (PFOA) electrochemically. We synthesized the monomer 3,4-ethylenedioxythiophene-2,2,6,6-tetramethylpiperidinyloxy (EDOT-TEMPO) for electropolymerization on a glassy carbon electrode using PFOA as a template, which was abbreviated as PEDOT-TEMPO-MIP. The redox-active MIP eliminated the need for external redox probes. When exposed to PFOA, both anodic and cathodic peaks of MIP showed a decreased current density. This observation can be explained by the formation of a charge-assisted hydrogen bond between the anionic PFOA and MIP's redox-active moieties (TEMPO) that hinder the conversion between the oxidized and reduced forms of TEMPO. The extent of the current density decrease showed excellent linearity with PFOA concentrations, with a method detection limit of 0.28 ng·L-1. PEDOT-TEMPO-MIP also exhibited high selectivity toward PFOA against other per- and polyfluoroalkyl substances (PFAS) at environmentally relevant concentrations. Our results suggest electropolymerization of MIPs was highly reproducible, with a relative standard deviation of 5.1% among three separate MIP electrodes. PEDOT-TEMPO-MIP can also be repeatedly used with good stability and reproducibility for PFOA detection. This study provides an innovative platform for rapid PFAS quantification using redox-active MIPs, laying the groundwork for developing compact PFAS sensors.

The efficiency of human fat products in wound healing: A systematic review and meta-analysis.

Wound development and healing involve intricate genetic and molecular processes, posing significant clinical management challenges. The objective of this study was to assess commonly used fat extracts' efficacy and safety (autologous fat, stromal vascular fraction and adipose-derived stem cells) in wound healing, particularly for refractory wounds, with the goal of providing evidence in clinical use. After a systematic review, 21 randomised controlled trials were included in our study. Based on the classification of human fat products, our meta-analysis revealed that the use of human fat products could speed healing rate, shorten healing time and achieve more complete healing, with statistically significant differences in outcome indicators when compared to conventional treatments. The analysis of histological findings across various studies indicated that fat extracts can promote epithelialization, collagen deposition and vascularization, thereby facilitating tissue regeneration and reducing inflammatory reactions. There were potential benefits to reducing patient pain levels after using adipose extracts. Furthermore, we analysed and summarised adverse events indicating the safe and effective clinical use of human fat products in wound treatment. Our research findings supported the efficiency of human fat products and demonstrated a high degree of safety in the clinical practice of wound management.

Up-regulation of miR-126 via DNA methylation in hypoxia-preconditioned endothelial cells may contribute to hypoxic tolerance of neuronal cells.

BACKGROUND: Endothelial cells (ECs) can confer neuroprotection by secreting molecules. This study aimed to investigate whether DNA methylation contributes to the neuroprotective gene expression induced by hypoxia preconditioning (HPC) in ECs and to clarify that the secretion of molecules from HPC ECs may be one of the molecular mechanisms of neuroprotection. METHODS: Human microvascular endothelial cell-1 (HMEC-1) was cultured under normal conditions (C), hypoxia(H), and hypoxia preconditioning (HPC), followed by the isolation of culture medium (CM). SY5Y cell incubated with the isolated CM from HMEC-1 was exposed to oxygen-glucose deprivation (OGD). The DNA methyltransferases (DNMTs), global methylation level, miR-126 and its promotor DNA methylation level in HMEC-1 were measured. The cell viability and cell injury in SY5Y were detected. RESULTS: HPC decreased DNMTs level and global methylation level as well as increased miR-126 expression in HMEC-1. CM from HPC treated HMEC-1 also relieved SY5Y cell damage, while CM from HMEC-1 which over-expression of miR-126 can reduce injury in SY5Y under OGD condition. CONCLUSIONS: These findings indicate EC may secrete molecules, such as miR-126, to execute neuroprotection induced by HPC through regulating the expression of DNMTs.

Ring finger protein 216 loss-of-function induces white matter hyperintensities by inhibiting oligodendroglia proliferation.

White matter hyperintensities (WMHs) refer to a group of diseases with numerous etiologies while oligodendrocytes remain the centerpiece in the pathogenesis of WMHs. Ring Finger Protein 216 (RNF216) encodes a ubiquitin ligase, and its mutation begets WMHs, ataxia, and cognitive decline in patients. Yet no study has revealed the function of RNF216 in oligodendroglia and WHIs before. In this study, we summarized the phenotypes of RNF216-mutation cases and explored the normal distribution of RNF216 in distinct brain regions and neuronal cells by bioinformatic analysis. Furthermore, MO3.13, a human oligodendrocyte cell line, was applied to study the function alteration after RNF216 knockdown. As a result, WMHs were the most common symptom in RNF216-mutated diseases, and RNF216 was indeed relatively enriched in corpus callosum and oligodendroglia in humans. The downregulation of RNF216 in oligodendroglia remarkably hampered cell proliferation by inhibiting the Akt pathway while having no significant effect on cell injury and oligodendrocyte maturation. Combining clinical, bioinformatical, and experimental evidence, our study implied the pivotal role of RNF216 in WMHs which might serve as a potent target in the therapy of WMHs.

Role of Nitrogenous Functional Group Identity in Accelerating 1,2,3-Trichloropropane Degradation by Pyrogenic Carbonaceous Matter (PCM) and Sulfide Using PCM-like Polymers.

Groundwater contamination by 1,2,3-trichloropropane (TCP) poses a unique challenge due to its human toxicity and recalcitrance to degradation. Previous work suggests that nitrogenous functional groups of pyrogenic carbonaceous matter (PCM), such as biochar, are important in accelerating contaminant dechlorination by sulfide. However, the reaction mechanism is unclear due, in part, to PCM's structural complexity. Herein, PCM-like polymers (PLPs) with controlled placement of nitrogenous functional groups [i.e., quaternary ammonium (QA), pyridine, and pyridinium cations (py+)] were employed as model systems to investigate PCM-enhanced TCP degradation by sulfide. Our results suggest that both PLP-QA and PLP-py+ were highly effective in facilitating TCP dechlorination by sulfide with half-lives of 16.91 ± 1.17 and 0.98 ± 0.15 days, respectively, and the reactivity increased with surface nitrogenous group density. A two-step process was proposed for TCP dechlorination, which is initiated by reductive ß-elimination, followed by nucleophilic substitution by surface-bound sulfur nucleophiles. The TCP degradation kinetics were not significantly affected by cocontaminants (i.e., 1,1,1-trichloroethane or trichloroethylene), but were slowed by natural organic matter. Our results show that PLPs containing certain nitrogen functional groups can facilitate the rapid and complete degradation of TCP by sulfide, suggesting that similarly functionalized PCM might form the basis for a novel process for the remediation of TCP-contaminated groundwater.

The adenosine A2A receptor in human sperm: its role in sperm motility and association with in vitro fertilization outcomes.

Background: The involvement of ATP and cAMP in sperm function has been extensively documented, but the understanding of the role of adenosine and adenosine receptors remains incomplete. This study aimed to examine the presence of adenosine A2A receptor (A2AR) and study the functional role of A2AR in human sperm. Methods: The presence and localization of A2AR in human sperm were examined by western blotting and immunofluorescence assays. The functional role of A2AR in sperm was assessed by incubating human sperm with an A2AR agonist (regadenoson) and an A2AR antagonist (SCH58261). The sperm level of A2AR was examined by western blotting in normozoospermic and asthenozoospermic men to evaluate the association of A2AR with sperm motility and in vitro fertilization (IVF) outcomes. Results: A2AR with a molecular weight of 43 kDa was detected in the tail of human sperm. SCH58261 decreased the motility, penetration ability, intracellular Ca2+ concentration, and CatSper current of human sperm. Although regadenoson did not affect these sperm parameters, it alleviated the adverse effects of SCH58261 on these parameters. In addition, the mean level of A2AR in sperm from asthenozoospermic men was lower than that in sperm from normozoospermic men. The sperm level of A2AR was positively correlated with progressive motility. Furthermore, the fertilization rate during IVF was lower in men with decreased sperm level of A2AR than in men with normal sperm level of A2AR. Conclusions: These results indicate that A2AR is important for human sperm motility and is associated with IVF outcome.

Chest non­contrasted computed tomography in detecting acute pulmonary thromboembolism: A single­center retrospective study.

The object of the study was to evaluate comprehensively the value of chest non-contrasted CT (NC-CT) in detecting acute pulmonary thromboembolism (APE). All patients were categorized into two groups: i) With APE; and ii) without APE based on clinical diagnosis. Using the clot distribution on computed tomography pulmonary angiography (CTPA), APE was divided into central and peripheral APE. Imaging features including hyperdense lumen sign and peripheral wedge-shaped opacity on chest NC-CT were evaluated. The attenuation value of peripheral wedge-shaped opacity on NC-CT was compared between patients with and without APE. Among the 273 patients, there were 110 patients with APE, 49 patients with central APE and 61 patients with peripheral APE and 163 patients without APE. The hyperdense lumen sign had a sensitivity of 30.0% and a specificity of 97.6% in detecting APE. The sensitivity and specificity of hyperdense lumen sign in detecting central APE were 57.1 and 97.6%, respectively, while the relevant percentages in detecting peripheral APE were 8.2 and 97.6%, respectively. The mean attenuation value of peripheral wedge-shaped opacity in patients with APE was significantly lower than that in patients without APE (P<0.001). Regarding the age-adjusted D-dimer, there was a decrease of eight D-dimer positive cases for patients >50 years old without APE, confirmed by CTPA. In conclusion, chest NC-CT cannot be used as an alternative modality for CTPA in diagnosing APE, however, the hyperdense lumen sign had high specificity in the diagnosis of central APE. Patients with this symptom and increased D-dimer may not require further CTPA. The lower attenuation value of peripheral wedge-shaped opacity on NC-CT suggested APE, and CTPA confirmation was required. The age-adjusted D-dimer had higher specificity in excluding APE.

Unraveling the Synergistic Mechanism of Ir Species with Various Electron Densities over an Ir/ZSM-5 Catalyst Enables High-Efficiency NO Reduction by CO.

Selective catalytic reduction using CO as a reducing agent (CO-SCR) has exhibited its application potential in coal-fired, steel, and other industrial sectors. In comparison to NH3-SCR, CO-SCR can achieve synergistic control of CO and NO pollutants, making it a powerful denitrification technology that treats waste with waste. Unfortunately, the competitive adsorption of O2 and NO on CO-SCR catalysts inhibits efficient conversion of NOx under O2-containing conditions. In this work, we obtained two Ir sites with different electron densities, Ir1 single atoms in the oxidized Irδ+ state and Ir0 nanoparticles in the metallic state, by controlled pretreatment of the Ir/ZSM-5 catalyst with H2 at 200 °C. The coexistence of Ir1 single atoms and Ir0 nanoparticles on ZSM-5 creates a synergistic effect, which facilitates the reduction of NO through CO in the presence of O2, following the Langmuir-Hinshelwood mechanism. The ONNO dimer is formed on the Ir1 single atom sites and then spills over to the neighboring Ir0 nanoparticles for subsequent reduction to N2 by CO. Specifically, this tandem reaction enables 83% NO conversion and 100% CO conversion on an Ir-based catalyst at 250 °C under 3% O2.

Acupoint catgut embedding attenuates oxidative stress and cognitive impairment in chronic cerebral ischemia by inhibiting the Ang II/AT1R/NOX axis.

Chronic cerebral ischemia (CCI) is a common neurological disorder, characterized by progressive cognitive impairment. Acupoint catgut embedding (ACE) represents a modern acupuncture form that has shown neuroprotective effects; nevertheless, its effects on CCI and the mechanisms remain largely unknown. Here, we aimed to explore the therapeutic action of ACE in CCI-induced cognitive impairment and its mechanisms. The cognitive function of CCI rats was determined using Morris water maze test, and histopathological changes in the brain were assessed through hematoxylin-eosin (HE) staining. To further explore the molecular mechanisms, the expression levels of oxidative stress markers and the Ang II/AT1R/NOX axis-associated molecules in the hippocampus were evaluated using enzyme-linked immunosorbent assay (ELISA), western blotting, and immunohistochemistry. Here, we observed that ACE treatment alleviated cognitive dysfunction and histopathological injury in CCI rats. Intriguingly, candesartan (an AT1R blocker) enhanced the beneficial effects of ACE on ameliorating cognitive impairment in CCI rats. Mechanistically, ACE treatment blocked the Ang II/AT1R/NOX pathway and subsequently suppressed oxidative stress, thus mitigating cognitive impairment in CCI. Our findings first reveal that ACE treatment could suppress cognitive impairment in CCI, which might be partly due to the suppression of Ang II/AT1R/NOX axis.

Experimental and Computational Study of Pyrogenic Carbonaceous Matter Facilitated Hydrolysis of 2,4-Dinitroanisole (DNAN).

This study investigated the reaction pathway of 2,4-dinitroanisole (DNAN) on the pyrogenic carbonaceous matter (PCM) to assess the scope and mechanism of PCM-facilitated surface hydrolysis. DNAN degradation was observed at pH 11.5 and 25 °C with a model PCM, graphite, whereas no significant decay occurred without graphite. Experiments were performed at pH 11.5 due to the lack of DNAN decay at pH below 11.0, which was consistent with previous studies. Graphite exhibited a 1.78-fold enhancement toward DNAN decay at 65 °C and pH 11.5 relative to homogeneous solution by lowering the activation energy for DNAN hydrolysis by 54.3 ± 3.9%. This is supported by our results from the computational modeling using Car-Parrinello simulations by ab initio molecular dynamics/molecular mechanics (AIMD/MM) and DFT free energy simulations, which suggest that PCM effectively lowered the reaction barriers by approximately 8 kcal mol-1 compared to a homogeneous solution. Quaternary ammonium (QA)-modified activated carbon performed the best among several PCMs by reducing DNAN half-life from 185 to 2.5 days at pH 11.5 and 25 °C while maintaining its reactivity over 10 consecutive additions of DNAN. We propose that PCM can affect the thermodynamics and kinetics of hydrolysis reactions by confining the reaction species near PCM surfaces, thus making them less accessible to solvent molecules and creating an environment with a weaker dielectric constant that favors nucleophilic substitution reactions. Nitrite formation during DNAN decay confirmed a denitration pathway, whereas demethylation, the preferred pathway in homogeneous solution, produces 2,4-dinitrophenol (DNP). Denitration catalyzed by PCM is advantageous to demethylation because nitrite is less toxic than DNAN and DNP. These findings provide critical insights for reactive adsorbent design that has broad implications for catalyst design and pollutant abatement.

MircoRNA-25-3p in skin precursor cell-induced Schwann cell-derived extracellular vesicles promotes axon regeneration by targeting Tgif1.

Nerve injury often leads to severe dysfunction because of the lack of axon regeneration in adult mammal. Intriguingly a series of extracellular vesicles (EVs) have the obvious ability to accelerate the nerve repair. However, the detailed molecular mechanisms to describe that EVs switch neuron from a transmitter to a regenerative state have not been elucidated. This study elucidated the microRNA (miRNA) expression profiles of two types of EVs that promote nerve regeneration. The functions of these miRNAs were screened in vitro. Among the 12 overlapping miRNAs, miR-25-3p was selected for further analysis as it markedly promoted axon regeneration both in vivo and in vitro. Furthermore, knockdown experiments confirmed that PTEN and Klf4, which are the major inhibitors of axon regeneration, were the direct targets of miR-25-3p in dorsal root ganglion (DRG) neurons. The utilization of luciferase reporter assays and functional tests provided evidence that miR-25-3p enhances axon regeneration by targeting Tgif1. Additionally, miR-25-3p upregulated the phosphorylation of Erk. Furthermore, Rapamycin modulated the expression of miR-25-3p in DRG neurons. Finally, the pro-axon regeneration effects of EVs were confirmed by overexpressing miR-25-3p and Tgif1 knockdown in the optic nerve crush model. Thus, the enrichment of miR-25-3p in EVs suggests that it regulates axon regeneration, proving a potential cell-free treatment strategy for nerve injury.

Nucleic-acid-base photofunctional cocrystal for information security and antimicrobial applications.

Cocrystal engineering is an efficient and simple strategy to construct functional materials, especially for the exploitation of novel and multifunctional materials. Herein, we report two kinds of nucleic-acid-base cocrystal systems that imitate the strong hydrogen bond interactions constructed in the form of complementary base pairing. The two cocrystals studied exhibit different colors of phosphorescence from their monomeric counterparts and show the feature of rare high-temperature phosphorescence. Mechanistic studies reveal that the strong hydrogen bond network stabilizes the triplet state and suppresses non-radiative transitions, resulting in phosphorescence even at 425 K. Moreover, the isolation effects of the hydrogen bond network regulate the interactions between the phosphor groups, realizing the manipulation from aggregation to single-molecule phosphorescence. Benefiting from the long-lived triplet state with a high quantum yield, the generation of reactive oxygen species by energy transfer is also available to utilize for some applications such as in photodynamic therapy and broad-spectrum microbicidal effects. In vitro experiments show that the cocrystals efficiently kill bacteria on a tooth surface and significantly help prevent dental caries. This work not only provides deep insight into the relationship of the structure-properties of cocrystal systems, but also facilitates the design of multifunctional cocrystal materials and enriches their potential applications.

The cyclimids: Degron-inspired cereblon binders for targeted protein degradation.

Cereblon (CRBN) is an E3 ligase substrate adapter widely exploited for targeted protein degradation (TPD) strategies. However, achieving efficient and selective target degradation is a preeminent challenge with ligands that engage CRBN. Here, we report that the cyclimids, ligands derived from the C-terminal cyclic imide degrons of CRBN, exhibit distinct modes of interaction with CRBN and offer a facile approach for developing potent and selective bifunctional degraders. Quantitative TR-FRET-based characterization of 60 cyclimid degraders in binary and ternary complexes across different substrates revealed that ternary complex binding affinities correlated strongly with cellular degradation efficiency. Our studies establish the unique properties of the cyclimids as versatile warheads in TPD and a systematic biochemical approach for quantifying ternary complex formation to predict their cellular degradation activity, which together will accelerate the development of ligands that engage CRBN.

Establishment of FDHSi003-A, a human induced pluripotent stem cell (hiPSC) line with a mutation of RNF216 c.1948G > T.

Gordon Holmes Syndrome (GDHS) is a hereditary neurodegenerative disease mainly associated with mutations of RNF216. We established a human induced pluripotent stem cell (hiPSC) line, FDHSi003-A, derived from PBMC of a patient baring a mutation of RNF216 c.1948G > T, who shows typical symptoms of GDHS. The generated FDHSi003-A expresses pluripotency markers, displays a normal karyotype, and has the potency to differentiate into all three germ layers. Thus, FDHSi003-A is an ideal model to investigate the mechanism of RNF216 in GDHS.

DTTZ suppresses ferroptosis and reverses mitochondrial dysfunction in normal tissues affected by chemotherapy.

Conventional antineoplastic therapies cause severe normal tissue damage and existing cytoprotectants with acute toxicities or potential tumor protection limit their clinical application. We evaluated the selective cytoprotection of 2,2-dimethylthiazolidine hydrochloride in this study, which could protect normal tissue toxicity without interfering antineoplastic therapies. By using diverse cell lines and A549 xenograft model, we discovered a synthetic aminothiol 2,2-dimethylthiazolidine hydrochloride selectively diminished normal cellular ferroptosis via SystemXc-/Glutathione Peroxidase 4 pathway upon antineoplastic therapies without interfering the anticancer efficacy. We revealed the malignant and non-malignant tissues presenting different energy metabolism patterns. And cisplatin induces disparate replicative stress, contributing to the distinguishable cytoprotection of 2,2-dimethylthiazolidine in normal and tumor cells. The compound pre-application could mitigate cisplatin-induced normal cellular mitochondrial oxidative phosphorylation (OXPHOS) dysfunction. Pharmacologic ablation of mitochondria reversed 2,2-dimethylthiazolidine chemoprotection against cisplatin in the normal cell line. Combined, these results provide a potential therapeutic adjuvant to selectively diminish normal tissue damages retaining antineoplastic efficacy.

circCPA4 induces malignant behaviors of prostate cancer via miR-491-5p/SHOC2 feedback loop.

OBJECTIVE: circCPA4 has been defined to be an oncogenic gene. This study examined whether circCPA4 regulates Prostate Cancer (PC) development and revealed its molecular mechanism. METHODS: PC tissues and PC cell lines were collected, in which circCPA4/miR-491-5p/SHOC2 levels were evaluated by RT-qPCR and immunoblot. Colony formation assay and EdU assay assessed cell proliferation, flow cytometry measured apoptosis, and Transwell assessed invasion and migration. Ki-67, cleaved caspase-3, E-cadherin, and N-cadherin were evaluated by immunoblot. Based on the luciferase reporter assay and RIP assay the authors investigated the targeting relationship between circCPA4/miR-491-5p/SHOC2. The effect of circCPA4 on tumor growth was evaluated by xenotransplantation in nude mice. RESULTS: circCPA4 and SHOC2 levels were abundant while miR-491-5p expression was low in PC. Loss of circCPA4 decreased the proliferation and EdU-positive rate of PC cells, enhanced apoptosis, and inhibited invasion, migration, and EMT. Upregulation of circCPA4 forced the malignant behaviors of PC cells, and this promotion could be abolished when miR-491-5p was overexpressed or SHOC2 was silenced. CircCAP4 competitively decoyed miR-491-5p mediating SHOC2 expression. circCAP4 suppression inhibited PC tumor growth. CONCLUSION: circCAP4 acts as a novel oncogenic factor in PC, accelerating the malignant behavior of PC cells via miR-491-5p/SHOC2 interaction. This novel ceRNA axis may be a potential target for PC drug development and targeted therapy in the future.

Role of automated functional imaging and myocardial work in assessment of cardiac function in children with obstructive sleep apnea.

BACKGROUND: Early identification of abnormal left ventricular function in children with obstructive sleep apnea (OSA) is difficult using conventional echocardiographic indices and commonly used clinical markers of myocardial damage. We sought to investigate the value of automatic function imaging and myocardial work parameters in predicting early cardiac impairment in children having OSA with preserved left heart function and thereby identifying an optimal index for assessment. PATIENTS AND METHODS: Fifty-two children who presented with symptoms of nocturnal sleep snoring and open-mouth breathing and 34 healthy controls were enrolled in this study. Clinical characteristics and conventional echocardiographic data were collected, and image analysis was performed using two-dimensional speckle-tracking echocardiography to obtain left ventricular global longitudinal strain (GLS), post-systolic index, peak strain dispersion, global work index (GWI), global constructive work (GCW), global wasted work, and global work efficiency. RESULTS: Children with OSA had significantly lower GLS, GWI, and GCW than those without (P < 0.05). Additionally, GWI (ß = -32.87, 95% CI: -53.47 to -12.27), and GCW (ß = -35.09, 95% CI: -55.35 to -14.84) were found to correlate with the disease severity in the multiple linear regression mode, with worsening values observed as the severity of the disease increased. ROC curve analysis revealed that GCW was the best predictor of myocardial dysfunction, with an AUC of 0.809 (P < 0.001), and the best cutoff point for diagnosing myocardial damage in children with OSA was 1965.5 mmHg%, with a sensitivity of 92.5% and a specificity of 58.7%. CONCLUSIONS: GLS, GWI, and GCW were identified as predictors of myocardial dysfunction in children with OSA, with GCW being the best predictor.