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  • 1
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    Online Resource
    The impact of early empirical antibiotics treatment on clinical outcome of very preterm infants: a nationwide multicentre study in China
    Springer Science and Business Media LLC ; 2023
    In:  Italian Journal of Pediatrics Vol. 49, No. 1 ( 2023-01-26)
    Details
    In: Italian Journal of Pediatrics, Springer Science and Business Media LLC, Vol. 49, No. 1 ( 2023-01-26)
    Abstract: Infants with rule-out infections are responsible for the majority of empirical antibiotics treatment (EAT) in neonatal intensive care units (NICUs), particularly very preterm infants (VPIs). Antibiotic overuse has been linked to adverse outcomes. There is a paucity of data on the association between EAT and clinical outcomes (containing the nutritional outcomes) of VPIs without infection-related morbidities. Methods Clinical data of VPIs admitted in 28 hospitals in 20 provinces of China from September 2019 to December 2020 were collected. EAT of VPIs was calculated as the number of days with initial usage in the first week after birth, and then categorized into 3 groups (antibiotic exposure: none, 1-4 days, and  〉  4 days). Clinical characteristics, nutritional status , and the short-term clinical outcomes among 3 groups were compared and analyzed. Results In total, 1834 VPIs without infection-related morbidities in the first postnatal week were enrolled, including 152 cases (8.3%) without antibiotics, 374 cases (20.4%) with EAT ≤4 days and 1308 cases (71.3%) with EAT 〉  4 days. After adjusting for the confounding variables, longer duration of EAT was associated with decreased weight growth velocity and increased duration of reach of full enteral feeding in EAT 〉  4 days group (a β : -4.83, 95% CI : − 6.12 ~ − 3.53; a β : 2.77, 95% CI : 0.25 ~ 5.87, respectively) than those receiving no antibiotics. In addition, the risk of feeding intolerance (FI) in EAT 〉  4 days group was 4 times higher than that in non-antibiotic group (a OR : 4.14, 95% CI : 1.49 ~ 13.56) and 1.8 times higher than that in EAT ≤4 days group (a OR : 1.82, 95% CI : 1.08 ~ 3.17). EAT 〉  4 days was also a risk factor for greater than or equal to stage 2 necrotizing enterocolitis (NEC) than those who did not receive antibiotics (a OR : 7.68, 95% CI : 1.14 ~ 54.75) and those who received EAT ≤4 days antibiotics (a OR : 5.42, 95% CI : 1.94 ~ 14.80). Conclusions The EAT rate among uninfected VPIs was high in Chinese NICUs. Prolonged antibiotic exposure was associated with decreased weight growth velocity, longer duration of reach of full enteral feeding, increased risk of feeding intolerance and NEC ≥ stage 2. Future stewardship interventions to reduce EAT use should be designed and implemented.
    Type of Medium: Online Resource
    ISSN: 1824-7288
    URL: Article
    DOI: 10.1186/s13052-023-01414-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2084688-5
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  • 2
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    DataSheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 12 ( 2022-1-6)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2022-1-6)
    Abstract: Immunotherapy, especially checkpoint inhibitors targeting PD-1 or PD-L1, has revolutionized cancer therapy. However, PD-1/PD-L1 inhibitors have not been investigated thoroughly in glioblastoma (GBM). Studies have shown that polymerase 1 and transcript release factor (PTRF/Cavin-1) has an immune-suppressive function in GBM. Thus, the relationship between PTRF and PD-L1 and their role in immune suppression requires further investigation in GBM. Methods We used public databases and bioinformatics analysis to investigate the relationship between PTRF and PD-L1. We next confirmed the predicted relationship between PTRF and PD-L1 in primary GBM cell lines by using different experimental approaches. RIP-Seq, RIP, ChIP, and qRT-PCR were conducted to explore the molecular mechanism of PTRF in immunosuppression. Results We found that PTRF stabilizes lncRNA NEAT1 to induce NF-κB and PD-L1 and promotes immune evasion in GBM. PTRF was found to correlate with immunosuppression in the public GBM databases. PTRF increased the level of PD-L1 in primary cell lines from GBM patients. We carried out RIP-Seq of GBM cells and found that PTRF interacts with lncRNA NEAT1 and stabilizes its mRNA. PTRF also promoted the activity of NF-κB by suppressing UBXN1 expression via NEAT1 and enhanced the transcription of PD-L1 through NF-κB activation. Finally, PTRF promoted immune evasion in GBM cells by regulating PD-1 binding and PD-L1 mediated T cell cytotoxicity. Conclusions In summary, our study identified the PTRF- NEAT1 -PD-L1 axis as a novel immune therapeutic target in GBM.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2021.802795
    DOI: 10.3389/fimmu.2021.802795.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 3
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    EPIC-0628 abrogates HOTAIR/EZH2 interaction and enhances the temozolomide efficacy via promoting ATF3 expression and inhibiting DNA damage repair in glioblastoma
    Elsevier BV ; 2024
    In:  Cancer Letters Vol. 588 ( 2024-04), p. 216812-
    Details
    In: Cancer Letters, Elsevier BV, Vol. 588 ( 2024-04), p. 216812-
    Type of Medium: Online Resource
    ISSN: 0304-3835
    URL: Article
    DOI: 10.1016/j.canlet.2024.216812
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 195674-7
    detail.hit.zdb_id: 2004212-7
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  • 4
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    A novel compound EPIC-0412 reverses temozolomide resistance via inhibiting DNA repair/MGMT in glioblastoma
    Oxford University Press (OUP) ; 2023
    In:  Neuro-Oncology Vol. 25, No. 5 ( 2023-05-04), p. 857-870
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 25, No. 5 ( 2023-05-04), p. 857-870
    Abstract: Temozolomide (TMZ) resistance has become an important obstacle affecting its therapeutic benefits. O6-methylguanine DNA methyltransferase (MGMT) is primarily responsible for the TMZ resistance in Glioblastoma multiforme (GBM) patients. In addition, active DNA damage repair pathways can also lead to TMZ resistance. Here, we reported a novel small-molecule inhibitor EPIC-0412 that improved the therapeutic efficacy of TMZ by & #x2028;inhibiting the DNA damage repair pathway and MGMT in GBM via epigenetic pathways. Methods The small-molecule compound EPIC-0412 was obtained through high-throughput screening. RNA immunoprecipitation (RIP), chromatin isolation by RNA purification (ChIRP), and chromatin immunoprecipitation (ChIP) assays were used to verify the effect of EPIC-0412. Co-immunoprecipitation (Co-IP) was used to elucidate the interactions of transcription factors at the MGMT promoter region. Animal experiments using a mouse model were performed to verify the efficacy of EPIC-0412 in sensitizing GBM cells to TMZ. Results EPIC-0412 physically interrupts the binding of HOTAIR and EZH2, leading to the upregulation of CDKN1A and BBC3, causing cell cycle arrest and apoptosis in GBM cells. EPIC-0412 inhibits DNA damage response in GBM cells through the p21-E2F1 DNA damage repair axis. EPIC-0412 epigenetically silences MGMT through its interaction with the ATF3-p-p65-HADC1 axis at the MGMT promoter region. The application of EPIC-0412 restored the TMZ sensitivity in GBM in vivo experiments. Conclusion This study discovered a small-molecule inhibitor EPIC-0412, which enhanced the chemotherapeutic effect of TMZ by acting on the p21-E2F1 DNA damage repair axis and ATF3-p-p65-MGMT axis, providing & #x2028;evidence for combining epigenetic drugs to increase the sensitization toward TMZ in GBM patients.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noac242
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 2094060-9
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  • 5
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    S-acylation of p62 promotes p62 droplet recruitment into autophagosomes in mammalian autophagy
    Elsevier BV ; 2023
    In:  Molecular Cell Vol. 83, No. 19 ( 2023-10), p. 3485-3501.e11
    Details
    In: Molecular Cell, Elsevier BV, Vol. 83, No. 19 ( 2023-10), p. 3485-3501.e11
    Type of Medium: Online Resource
    ISSN: 1097-2765
    URL: Article
    DOI: 10.1016/j.molcel.2023.09.004
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 2001948-8
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  • 6
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    EPIC-1042 as a potent PTRF/Cavin1–caveolin-1 interaction inhibitor to induce PARP1 autophagic degradation and suppress temozolomide efflux for glioblastoma
    Oxford University Press (OUP) ; 2023
    In:  Neuro-Oncology ( 2023-08-31)
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), ( 2023-08-31)
    Abstract: Temozolomide (TMZ) treatment efficacy in glioblastoma is determined by various mechanisms such as TMZ efflux, autophagy, base excision repair (BER) pathway, and the level of O6-methylguanine-DNA methyltransferase (MGMT). Here, we reported a novel small-molecular inhibitor (SMI) EPIC-1042 (C20H28N6) with the potential to decrease TMZ efflux and promote PARP1 degradation via autolysosomes in the early stage. Methods EPIC-1042 was obtained from receptor-based virtual screening. Co-immunoprecipitation and pull-down assays were applied to verify the blocking effect of EPIC-1042. Western blotting, co-immunoprecipitation, and immunofluorescence were used to elucidate the underlying mechanisms of EPIC-1042. In vivo experiments were performed to verify the efficacy of EPIC-1042 in sensitizing glioblastoma cells to TMZ. Results EPIC-1042 physically interrupted the interaction of PTRF/Cavin1 and caveolin-1, leading to reduced secretion of small extracellular vesicles (sEVs) to decrease TMZ efflux. It also induced PARP1 autophagic degradation via increased p62 expression that more p62 bound to PARP1 and specially promoted PARP1 translocation into autolysosomes for degradation in the early stage. Moreover, EPIC-1042 inhibited autophagy flux at last. The application of EPIC-1042 enhanced TMZ efficacy in glioblastoma in vivo. Conclusion EPIC-1042 reinforced the effect of TMZ by preventing TMZ efflux, inducing PARP1 degradation via autolysosomes to perturb the BER pathway and recruitment of MGMT, and inhibiting autophagy flux in the later stage. Therefore, this study provided a novel therapeutic strategy using the combination of TMZ with EPIC-1042 for glioblastoma treatment.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noad159
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
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  • 7
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    Phosphatidylcholine‐Engineered Exosomes for Enhanced Tumor Cell Uptake and Intracellular Antitumor Drug Delivery
    Wiley ; 2021
    In:  Macromolecular Bioscience Vol. 21, No. 8 ( 2021-08)
    Details
    In: Macromolecular Bioscience, Wiley, Vol. 21, No. 8 ( 2021-08)
    Abstract: Exosomes derived from non‐tumor cells hold great potential as drug delivery vehicles because of their good biosafety and natural transference of bioactive cargo between cells. However, compared to tumor‐derived exosomes, efficient delivery is limited by their weak interactions with tumor cells. It is essential to engineer exosomes that improve tumor cellular internalization efficiency. A simple and effective strategy to enhance tumor cell uptake by engineering the exosome membrane lipids can be established by drawing on the role of lipids in tumor exosomes interacting with tumor cells. Amphiphilic phosphatidylcholine (PC) molecules are inserted into the membrane lipid layer of reticulocyte‐derived exosomes (Exos) by simple incubation to construct PC‐engineered exosomes (PC‐Exos). It is demonstrated that PC‐Exos showed significantly enhanced tumor cell internalization and uptake rate compared to native Exos, up to a twofold increase. After therapeutic agent loading, PC‐Exos remarkably promotes intracellular drug or RNA accumulation in cancer cells, thus showing enhanced in vitro anti‐tumor activity. This work demonstrates the crucial role of engineering exosomal lipids in modulating cancer cellular uptake, which may shed light on the design of high‐efficiency exosome‐based drug delivery carriers.
    Type of Medium: Online Resource
    ISSN: 1616-5187 , 1616-5195
    URL: Issue
    URL: Article
    DOI: 10.1002/mabi.v21.8
    DOI: 10.1002/mabi.202100042
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2039130-4
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  • 8
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    Efficiency Evaluation and Analysis of Low-Carbon Tourism and Ecological Construction Based on DEA Model
    Hindawi Limited ; 2022
    In:  Mathematical Problems in Engineering Vol. 2022 ( 2022-7-30), p. 1-10
    Details
    In: Mathematical Problems in Engineering, Hindawi Limited, Vol. 2022 ( 2022-7-30), p. 1-10
    Abstract: The rapid development of tourism in China has also caused a lot of energy consumption and serious environmental problems. In the context of sustainable development, low-carbon tourism has become the consensus of management departments, relevant industries, and academia. In environmental-related fields, DEA is considered as an excellent efficiency analysis tool because of its powerful optimization ability. The final variable of DEA method is weight. In order to avoid the influence of human factors with predetermined weights in tourism analysis, this paper studies the evaluation of tourism ecological efficiency based on DEA model. China’s overall tourism ecological efficiency showed a fluctuating upward trend, rising from 0.853 in 2018 to 0.906 in 2021. The national average efficiency over the past four years is 0.855, which is at a low level, indicating that the construction of tourism ecology is still in its infancy, and there is still much room for improvement in the future. As the tourism industry system involves many aspects, such as natural ecology, humanities, economy, and so on, it is an extremely complex system. The research on the ecological efficiency of tourism cannot simply rely on the knowledge system and thinking of a single discipline. Therefore, combined with the relevant theories and knowledge of tourism, management, industrial economics, regional economics, industrial ecology, and other disciplines, this paper makes a systematic study on the problems and countermeasures of Qiaozhai.
    Type of Medium: Online Resource
    ISSN: 1563-5147 , 1024-123X
    URL: Article
    DOI: 10.1155/2022/1218900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2014442-8
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  • 9
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    Anatomical and chemical characteristics associated with lodging resistance in wheat
    Elsevier BV ; 2013
    In:  The Crop Journal Vol. 1, No. 1 ( 2013-10), p. 43-49
    Details
    In: The Crop Journal, Elsevier BV, Vol. 1, No. 1 ( 2013-10), p. 43-49
    Type of Medium: Online Resource
    ISSN: 2214-5141
    URL: Article
    DOI: 10.1016/j.cj.2013.07.012
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2013
    detail.hit.zdb_id: 2745450-2
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  • 10
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    GFAP hyperpalmitoylation exacerbates astrogliosis and neurodegenerative pathology in PPT1-deficient mice
    Proceedings of the National Academy of Sciences ; 2021
    In:  Proceedings of the National Academy of Sciences Vol. 118, No. 13 ( 2021-03-30)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 118, No. 13 ( 2021-03-30)
    Abstract: The homeostasis of protein palmitoylation and depalmitoylation is essential for proper physiological functions in various tissues, in particular the central nervous system (CNS). The dysfunction of PPT1 (PPT1-KI, infantile neuronal ceroid lipofuscinosis [INCL] mouse model), which catalyze the depalmitoylation process, results in serious neurodegeneration accompanied by severe astrogliosis in the brain. Endeavoring to determine critical factors that might account for the pathogenesis in CNS by palm-proteomics, glial fibrillary acidic protein (GFAP) was spotted, indicating that GFAP is probably palmitoylated. Questions concerning if GFAP is indeed palmitoylated in vivo and how palmitoylation of GFAP might participate in neural pathology remain unexplored and are waiting to be investigated. Here we show that GFAP is readily palmitoylated in vitro and in vivo; specifically, cysteine-291 is the unique palmitoylated residue in GFAP. Interestingly, it was found that palmitoylated GFAP promotes astrocyte proliferation in vitro. Furthermore, we showed that PPT1 depalmitoylates GFAP, and the level of palmitoylated GFAP is overwhelmingly up-regulated in PPT1-knockin mice, which lead us to speculate that the elevated level of palmitoylated GFAP might accelerate astrocyte proliferation in vivo and ultimately led to astrogliosis in INCL. Indeed, blocking palmitoylation by mutating cysteine-291 into alanine in GFAP attenuate astrogliosis, and remarkably, the concurrent neurodegenerative pathology in PPT1-knockin mice. Together, these findings demonstrate that hyperpalmitoylated GFAP plays critical roles in regulating the pathogenesis of astrogliosis and neurodegeneration in the CNS, and most importantly, pinpointing that cysteine-291 in GFAP might be a valuable pharmaceutical target for treating INCL and other potential neurodegenerative diseases.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2022261118
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2021
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    detail.hit.zdb_id: 1461794-8
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