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Efferocytosis refers to the process by which phagocytes remove apoptotic cells and related apoptotic products. It is essential for the growth and development of the body, the repair of damaged or inflamed tissues, and the balance of the immune system. Damaged efferocytosis will cause a variety of chronic inflammation and immune system diseases. Many studies show that efferocytosis is a process mediated by mitochondria. Mitochondrial metabolism, mitochondrial dynamics, and communication between mitochondria and other organelles can all affect phagocytes' clearance of apoptotic cells. Therefore, targeting mitochondria to modulate phagocyte efferocytosis is an anticipated strategy to prevent and treat chronic inflammatory diseases and autoimmune diseases. In this review, we introduced the mechanism of efferocytosis and the pivoted role of mitochondria in efferocytosis. In addition, we focused on the therapeutic implication of drugs targeting mitochondria in diseases related to efferocytosis dysfunction.

Cardiovascular disease is the leading cause of death worldwide, and it's of great importance to understand its underlying mechanisms and find new treatments. Sphingosine 1-phosphate (S1P) is an active lipid that exerts its effects through S1P receptors on the cell surface or intracellular signal, and regulates many cellular processes such as cell growth, cell proliferation, cell migration, cell survival, and so on. S1PR modulators are a class of modulators that can interact with S1PR subtypes to activate receptors or block their activity, exerting either agonist or functional antagonist effects. Many studies have shown that S1P plays a protective role in the cardiovascular system and regulates cardiac physiological functions mainly through interaction with cell surface S1P receptors (S1PRs). Therefore, S1PR modulators may play a therapeutic role in cardiovascular diseases. Here, we review five S1PRs and their functions and the progress of S1PR modulators. In addition, we focus on the effects of S1PR modulators on atherosclerosis, myocardial infarction, myocardial ischaemia/reperfusion injury, diabetic cardiovascular diseases, and myocarditis, which may provide valuable insights into potential therapeutic strategies for cardiovascular disease.

Objective: Transfer RNA-derived fragments (tRFs) are short non-coding RNA (ncRNA) sequences, ranging from 14 to 30 nucleotides, produced through the precise cleavage of precursor and mature tRNAs. While tRFs have been implicated in various diseases, including cancer, their role in lung adenocarcinoma (LUAD) remains underexplored. This study aims to investigate the impact of tRF-Val-CAC-010, a specific tRF molecule, on the phenotype of LUAD cells and its role in tumorigenesis and progression in vivo., Methods: The expression level of tRF-Val-CAC-010 was quantified using quantitative real-time polymerase chain reaction (qRT-PCR). Specific inhibitors and mimics of tRF-Val-CAC-010 were synthesized for transient transfection. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8), while cell invasion and migration were evaluated through Transwell invasion and scratch assays. Flow cytometry was utilized to analyze cell cycle and apoptosis. The in vivo effects of tRF-Val-CAC-010 on tumor growth and metastasis were determined through tumor formation and metastasis imaging experiments in nude mice., Results: The expression level of tRF-Val-CAC-010 was upregulated in A549 and PC9 LUAD cells (P < 0.01). Suppression of tRF-Val-CAC-010 expression resulted in decreased proliferation of A549 and PC9 cells (P < 0.001), reduced invasion and migration of A549 (P < 0.05, P < 0.001) and PC9 cells (P < 0.05, P < 0.01), enhanced apoptosis in both A549 (P < 0.05) and PC9 cells (P < 0.05), and increased G2 phase cell cycle arrest in A549 cells (P < 0.05). In vivo, the tumor formation volume in the tRF-inhibitor group was significantly smaller than that in the model and tRF-NC groups (P < 0.05). The metastatic tumor flux value in the tRF-inhibitor group was also significantly lower than that in the model and tRF-NC groups (P < 0.05)., Conclusion: This study demonstrates that tRF-Val-CAC-010 promotes proliferation, migration, and invasion of LUAD cells and induces apoptosis in vitro, however, its specific effects on the cell cycle require further elucidation. Additionally, tRF-Val-CAC-010 enhances tumor formation and metastasis in vivo. Therefore, tRF-Val-CAC-010 may serve as a novel diagnostic biomarker and potential therapeutic target for LUAD., (© 2024. The Author(s).)

The supramolecular lead iodide perovskite crystals, {[NH 4 (18-crown-6)]PbI 3 } ∞ (1), (18-crown-6 = 1,4,7,10,13,16-hexaoxacyclooctadecane), was successfully achieved by a facile solvent evaporation strategy using a DMF solution containing equal molar quantities of PbI 2 , NH 4 I and 18-crown-6. The supramolecular perovskite was characterized by microanalysis for C, H and N elements, thermogravimetric (TG) analysis, differential scanning calorimetry (DSC), powder X-ray diffraction (PXRD) and single crystal X-ray diffraction techniques. DSC measurements demonstrated that 1 experiences a two-step thermotropic phase transition around 333 K and 383 K, respectively. The phase transition is relevant to the disorder-order transformation of the 18-crown-6 molecule at ∼333 K, while both breaking-symmetry and ordered-disordered transformation of the 18-crown-6 molecule occurred at ∼383 K. In addition, the sharp change of the PbI 6 coordination octahedron distortion degree plays a synergistic role in the two-step phase transition. The dielectric relaxation occurs above 243 K in 1 and is mainly attributed to the displacement of the NH 4 + ions relative to the ring of the 18-crown-6 molecule and {PbI 3 } ∞ chain induced by an AC electrical field.

This study aimed to compare the application value of capillary electrophoresis and next-generation sequencing for immunoglobulin (IG) gene rearrangement in the diagnosis of classic Hodgkin's lymphoma. Twenty paraffin-embedded specimens from patients with classic Hodgkin's lymphoma were screened. For gene rearrangement detection, the ABI 3500 Genetic Analyzer and ABI Ion GeneStudio S5 Plus sequencing system were used, respectively, and the results were compared. Five cases with monoclonal rearrangements (25%, 5/20) were detected by Capillary Electrophoresis, and positivity for the FR1, FR2, FR3, and IGк loci was 5%, 10%, 10%, and 15%, respectively; 12 cases with monoclonal rearrangements (60%, 12/20) were detected by Next-generation Sequencing where the positivity of the above corresponding loci were 35%, 45%, 50%, and 30%, respectively. Among the 20 samples, 6 IGк clonal rearrangements were detected, and the usage frequency (66.7%) of IGкJ4 was the highest in the IGкJ subgroup. The usage frequency of IGкV1 and IGкV3 in the GкV sub-group was 33.3% and 33.3%, respectively. Twelve immunoglobulin heavy chain (IGH) clonal rearrangements were detected among the 20 samples, and the order of usage frequency in the IGH joining region J (IGHJ) subgroup was IGHJ4 > IGHJ5 > IGHJ6 > IGHJ3. The gene with the highest usage frequency in the IGH variable (IGHV) subgroup was IGHV3 (50%) and the percentage of IGHV mutations ranged from 0% ± 11.45% with an average frequency of 3.34%. Compared with Capillary Electrophoresis, Next-generation Sequencing showed a higher positivity in the detection of gene clonal rearrangements, was more accurate in the interpretation of results.

Ischemia-reperfusion injury is a complex hemodynamic pathology that is a leading cause of death worldwide and occurs in many body organs. Numerous studies have shown that mitochondria play an important role in the occurrence mechanism of ischemia-reperfusion injury and that mitochondrial structural abnormalities and dysfunction lead to the disruption of the homeostasis of the whole mitochondria. At this time, mitochondria are not just sub-organelles to produce ATP but also important targets for regulating ischemia-reperfusion injury; therefore, drugs targeting mitochondria can serve as a new strategy to treat ischemia-reperfusion injury. Based on this view, in this review, we discuss potential therapeutic agents for both mitochondrial structural abnormalities and mitochondrial dysfunction, highlighting the application and prospects of targeted mitochondrial drugs in the treatment of ischemia-reperfusion injury, and try to provide new ideas for the clinical treatment of the ischemia-reperfusion injury., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To generate immunity against human papillomavirus (HPV), the use of a recombinant DNA vaccine to carry an appropriate target gene is a promising and cost-effective approach. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent immunomodulatory cytokine that enhances the efficacy of vaccines by promoting the development and prolongation of humoral and cellular immunity. In this study, we linked codon-optimized GM-CSF (cGM-CSF) to the HPV16 E7 sequence as fused protein and evaluated the immunogenic potential of this DNA vaccine., Materials and Methods: We have demonstrated that cGM-CSF enhanced immunity against tumor challenges by generating and promoting the proliferation of HPV16 E7-specific CD8+ T cells, which secrete IFN-γ in the murine model. In this study, we aimed to evaluate the immunogenic potential of DNA vaccine that constructed by linking codon-optimized GM-CSF to HPV16 E7 sequence in the animal model. We study the half-life of RNA decay and cellular location of HPV16 E7 by Q-PCR and Western blot. We also assess immune response in the animal model by flow cytometry and ELISA., Results: The cGM-CSF-E7 sequence increased and extended the expression of E7 mRNA, in comparison with the E7 sequence alone. Mice vaccinated with the cGM-CSF-E7 DNA vaccine exhibited a slower rate of tumor growth than those vaccinated with the unconjugated E7 DNA vaccine. We also found that the CD4 and CD8+ T cells from these mice showed strong secretion of IFN-γ., Conclusion: Through in vivo antibody depletion experiments, we demonstrated that both CD4+ and CD8+ T cells play an important role in the suppression of tumor growth., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2021. Published by Elsevier B.V.)

Background: Gastrointestinal (GI) hemangioma has a low incidence among systemic hemangiomas, and some GI hemangiomas occur in the intestine, stomach, and esophagus. Polidocanol has been increasingly used in sclerotherapy. However, this paper reports that minimally invasive treatment of multiple hemangiomas with large diameters can achieve satisfactory results by multipoint injection., Case Summary: A 46-year-old female patient was hospitalized in another hospital for cough. We accidentally found thickening of the lower esophagus by chest computed tomography. The patient was eventually diagnosed with multiple GI hemangiomas and underwent a series of examinations including esophagogastroduodenoscopy (EGD), endoscopic ultrasound, and magnetic resonance imaging. We calculated the dose of polidocanol according to the volumes of the hemangiomas, fixed the target vein with the help of a transparent cap, and then administered polidocanol via multipoint injection into the hemangiomas under endoscopic guidance. EGD and endoscopic ultrasound showed that the hemangiomas disappeared. The color of the esophageal mucosa returned to normal 1 mo after sclerotherapy., Conclusion: Sclerotherapy may be a safe and effective method for treating multiple hemangiomas of the alimentary canal., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest to report., (©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.)

Lactic acid bacteria (LAB) are an important group of microorganisms in the food industry. LAB with health benefits are considered natural elements promoting consumer health. The study investigated the anti-obesity effects of Lactobacillus plantarum CQPC01 (LP-CQPC01) on high-fat diet-induced mice. Liver morphology, liver function indexes, lipid indexes, and inflammatory factors in the serum and liver were determined. Expressions of lipid metabolism-related gene were also detected by qPCR. LP-CQPC01 slowed the HFD-induced increase in body weight, decreased the organ indexes, alleviated hepatic lipid accumulation, and inhibited the increased adipose cell volume. LP-CQPC01 decreased lipid levels of serum and liver, and the contents of pro-inflammatory factors, and increased the IL-4 and IL-10 contents. LP-CQPC01 downregulated the expressions of the C/EBP-α and PPARγ mRNA and upregulated CYP7A1, CPT1, LPL, CAT, SOD1, and SOD2 mRNA. Our results indicated that LP-CQPC01 is a potential probiotic for preventing or alleviating high-energy intake-related lipid conditions. PRACTICAL APPLICATIONS: Obesity is a factor of a variety of cardiovascular diseases. Therefore, it is necessary to suppress the occurrence of fat accumulation in time. This study investigated the effect of LP-CQPC01 on lipid regulation in mice fed a high-fat diet (HFD) and clarified the mechanism of strain to alleviate obesity by enhancing the decomposition of cholesterol and detoxification of fat. LP-CQPC01 reduced fat accumulation without oxidative damage, and was confirmed by the attenuated pathological changes of liver. This research can serve as a significant reference for future research, prevention, and treatment of high-energy intake-related lipid conditions, and the development of functional foods with anti-obesity activity., (© 2020 Wiley Periodicals LLC.)

Direct ethylene glycol fuel cells (DEGFCs) and water splitting devices have received intensive interest during the past few decades. However, the commonly used Pt catalysts are seriously restricted by the high cost and very low resistance to CO-like intermediates during the catalysis. Herein, a general and simple solvothermal method was developed to synthesize three-dimensional (3D) bimetallic alloyed PtRh nanodendrites (NDs) for ethylene glycol oxidation reaction (EGOR) and hydrogen evolution reaction (HER). Citric acid (CA) and cetyltrimethylammonium chloride (CTAC) played important roles in formation of such dendritic structures. The optimized Pt 56 Rh 44 NDs displayed the greatest mass activity (MA) for EGOR in 0.5 M KOH, which was 2.6-fold higher than commercial Pt black, coupled with the remarkable increase in the HER activity with a decayed overpotential of 20.0 mV to drive a current density of 10 mA cm -2 relative to the homemade Pt 41 Rh 59 NDs (26.2 mV), Pt 81 Rh 19 NDs (26.2 mV), Pt black (44.3 mV), Pt/C (44.4 mV) and Rh NFs (37.3 mV). This work offers some constructive guidelines for synthesis of advanced Pt-based catalysts in such energy devices., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

An erratum is presented to correct equation (8) in [Opt. Express25(23), 28710 (2017).10.1364/OE.25.028710].

Objective: To determine the effect of downregulation of 53BP1 expression on cell growth and radiosensitivity in laryngeal carcinoma Hep-2 cells., Methods: HEP-2 cell lines were established with a stable knockdown of 53BP1 with short hairpin RNA (shRNA). The level of expressed protein of negative control group (NC),wild type Hep-2 and downregulation of 53BP1 (P6) group was determined by Western blotting. Proliferation on normal conditions was detected by MTT. Radiosensitivity and growth of cells were detected by flow cytometry., Results: A stable 53BP1 downregulated cell line P6 was established. Similar cell growth was observed between the 53BP1 downregulated cells and the control cells. The downregulation of 53BP1 reduced the number of clonogenic cells exposed to radiation. Compared with wild type Hep-2 group and NC group, Western blot results showed a decrease in 53BP1 protein level in P6 group (P < 0.05), reducing the ratio of arrest of G2/M with radiation dose increased (P < 0.05). MTT results revealed the lower 53BP1 protein level did not affect the cell proliferation. After exposure to 0, 2, 6, 10 Gy ionizing radiation (IR), P6 cells had lower, radiosensitivity parameters (D0, SF2, Dq, N) than controls and wild type Hep-2 (P < 0.05)., Conclusion: RNA interference could effectively down-regulate the expression of 53BP1 and reduce arrest of G2/M phase, thus enhancing the radiosensitivity of Hep-2 cell line.