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  • Ovid Technologies (Wolters Kluwer Health)  (7)
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  • Ovid Technologies (Wolters Kluwer Health)  (7)
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  • 1
    In: AIDS, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 6 ( 2021-05-1), p. 851-860
    Abstract: Despite successful antiviral therapy, the recovery of CD4 + T cells may not be complete in certain HIV-1-infected individuals. In our previous work with humanized mice infected with CXCR4-tropic HIV-1 LAI (LAI), viral protein Nef was found the major factor determining rapid loss of both CD4 + T cells and CD4 + CD8 + thymocytes but its effect on early T-cell development is unknown. The objective of this study is to investigate the influence of LAI Nef on the development of hematopoietic stem/progenitor cells (HSPCs) into T lymphoid cells. Design: HSPC-OP9-DL1 cell co-culture and humanized mouse model was used to investigate the objective of our study in vitro and in vivo . RNA-seq was exploited to study the change of gene expression signature after nef expression in HSPCs. Results: Nef expression in HSPCs was found to block their development into T lymphoid cells both in vitro and in the mice reconstituted with n ef -expressing HSPCs derived from human cord blood. More surprisingly, in humanized mice nef expression preferentially suppressed the production of CD4 + T cells. This developmental defect was not the result of CD34+ cell loss. RNA-seq analysis revealed that Nef affected the expression of 176 genes in HSPCs, including those involved in tumor necrosis factor, Toll-like receptor, and nucleotide-binding oligomerization domain-like receptor signaling pathways that are important for hematopoietic cell development. Conclusion: Our results demonstrate that Nef compromises the development of HSPCs into T lymphoid cells, especially CD4 + T cells. This observation suggests that therapeutics targeting Nef may correct HIV-1-associated hematopoietic abnormalities, especially defects in T-cell development.
    Type of Medium: Online Resource
    ISSN: 0269-9370 , 1473-5571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2012212-3
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  • 2
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 4 ( 2023-04), p. 504-518
    Abstract: Angiogenesis is a promising strategy for those with peripheral artery disease. Macrophage-centered inflammation is intended to govern the deficiency of the angiogenic response after hindlimb ischemia. However, little is known about the mechanism of macrophage activation beyond signals from cytokines and chemokines. We sought to identify a novel mechanical signal from the ischemic microenvironment that provokes macrophages and the subsequent inflammatory cascade and to investigate the potential role of Piezo-type mechanosensitive ion channels (Piezo) on macrophages during this process. Methods: Myeloid cell-specific Piezo1 (Piezo-type mechanosensitive ion channel component 1) knockout ( Piezo1 ΔMΦ ) mice were generated by crossing Piezo1 fl/fl ( LysM-Cre −/− ; Piezo1 flox/flox ) mice with LysM-Cre transgenic mice to assess the roles of Piezo1 in macrophages after hindlimb ischemia. Furthermore, in vitro studies were carried out in bone marrow–derived macrophages to decipher the underlying mechanism. Results: We found that tissue stiffness gradually increased after hindlimb ischemia, as indicated by Young’s modulus. Compared to Piezo2, Piezo1 expression and activation were markedly upregulated in macrophages from ischemic tissues in concurrence with increased tissue stiffness. Piezo1 ΔMΦ mice exhibited improved perfusion recovery by enhancing angiogenesis. Matrigel tube formation assays revealed that Piezo1 deletion promoted angiogenesis by enhancing FGF2 (fibroblast growth factor-2) paracrine signaling in macrophages. Conversely, activation of Piezo1 by increased stiffness or the agonist Yoda1 led to reduced FGF2 production in bone marrow–derived macrophages, which could be blocked by Piezo1 silencing. Mechanistically, Piezo1 mediated extracellular Ca 2+ influx and activated Ca 2+ -dependent CaMKII (calcium/calmodulin-dependent protein kinase II)/ETS1 (ETS proto-oncogene 1) signaling, leading to transcriptional inactivation of FGF2. Conclusions: This study uncovers a crucial role of microenvironmental stiffness in exacerbating the macrophage-dependent deficient angiogenic response. Deletion of macrophage Piezo1 promotes perfusion recovery after hindlimb ischemia through CaMKII/ETS1-mediated transcriptional activation of FGF2. This provides a promising therapeutic strategy to enhance angiogenesis in ischemic diseases.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1494427-3
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  NeuroReport Vol. 31, No. 1 ( 2020-01-8), p. 64-68
    In: NeuroReport, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 1 ( 2020-01-8), p. 64-68
    Abstract: The hippocampus in neonatal rats is not fully developed after birth, and the effect of odor-aversion learning on memory consolidation in the immature hippocampus is not well understood. Therefore, the aim of the present study was to explore the effects of odor-aversion learning in neonatal rats on memory consolidation and neurodevelopment in the immature hippocampus. The effect of hippocampal-induced learning was measured at two different developmental stages using the Y-maze and c-Fos protein levels. Furthermore, hippocampal cell proliferation and growth-associated protein 43 (GAP-43) expression were evaluated at different developmental stages, namely, postnatal day 7 (PN7) and PN24, after odor-aversion learning. Both PN7 and PN24 rats avoided conditioned odor stimuli after odor-aversion learning. PN7 and PN24 rats in the odor-averse learning groups exhibited high c-Fos protein levels. PN7 rats exhibited high cell proliferation rates and GAP-43 protein levels after odor-aversion learning. These results showed that the immature hippocampus can participated in odor-aversion learning, which may induce cell proliferation and axonal development.
    Type of Medium: Online Resource
    ISSN: 0959-4965
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2031485-1
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Cornea Vol. 36, No. 7 ( 2017-07), p. 841-844
    In: Cornea, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 7 ( 2017-07), p. 841-844
    Abstract: The expression of peroxiredoxin 2 and vascular endothelial growth factor receptor 2 (VEGFR2) was detected in pterygium to investigate whether they are involved in the pathogenesis or recurrence of pterygium and to evaluate the association between peroxiredoxin 2 and VEGFR2 in pterygium. Methods: Ten normal bulbar conjunctivae, 35 primary pterygia, and 35 recurrent pterygia were obtained. Formalin-fixed, paraffin-wax–embedded tissues were analyzed by immunohistochemistry with peroxiredoxin 2 and VEGFR2 antibodies. Results: There was no statistical difference between primary pterygia and recurrent pterygia in terms of age and sex ( P = 0.685; P = 0.811). The expression rate of peroxiredoxin 2 (94.3%, 66/70) and VEGFR2 (61.4%, 43/70) was increased in pterygia compared with normal conjunctivae (negative). The expression of peroxiredoxin 2 in recurrent pterygia (negative 0, weak 0, moderate 27, strong 8) was higher than that in primary pterygia (negative 6, weak 16, moderate 13, strong 0) ( P 〈 0.001). The expression of VEGFR2 in recurrent pterygia (negative 4, weak 5, moderate 12, strong 4) was higher than that in primary pterygia (negative 23, weak 10, moderate 1, strong 1) ( P 〈 0.001). The expression of peroxiredoxin 2 was consistent with that of VEGFR2 in pterygium ( r = 0.348, P = 0.006). Conclusions: Overexpression of peroxiredoxin 2 and VEGFR2 in pterygium might be involved in the pathogenesis or recurrence of pterygium. The increase of VEGFR2 might be related to the increase of peroxiredoxin 2 in response to excessive reactive oxygen species from ultraviolet exposure.
    Type of Medium: Online Resource
    ISSN: 0277-3740
    RVK:
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2045943-9
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  • 5
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 5 ( 2014-11), p. 440-447
    Type of Medium: Online Resource
    ISSN: 1073-2322
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2011863-6
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  • 6
    In: Chinese Medical Journal, Ovid Technologies (Wolters Kluwer Health), Vol. 135, No. 21 ( 2022-10-12), p. 2617-2619
    Type of Medium: Online Resource
    ISSN: 0366-6999 , 2542-5641
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2108782-9
    SSG: 6,25
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  • 7
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Clinical Spine Surgery: A Spine Publication Vol. 31, No. 4 ( 2018-05), p. 180-184
    In: Clinical Spine Surgery: A Spine Publication, Ovid Technologies (Wolters Kluwer Health), Vol. 31, No. 4 ( 2018-05), p. 180-184
    Abstract: Descriptive study. Objectives: This study aimed to evaluate the hidden blood loss (HBL) of patients who underwent lumbar fusion surgery for degenerative spine and to analyze its risk factors. Summary of Background Data: When planning transfusion strategies, blood loss calculation is important. However, in clinical practice, spine surgeons usually ignore the possibility that a large amount of HBL may occur after lumbar fusion surgery. Materials and Methods: We studied the patients who underwent posterior lumbar fusion (PLF) surgery for degenerative spine from 2014 to 2015 in one institution. The patient’s demographics, comorbid conditions, coagulation panel value, surgical time, number of levels fused, American Society of Anesthesiologists (ASA) classification, cell saver, preoperative hematocrit level, preoperative hemoglobin level, and postoperative complications were collected retrospectively. Pearson correlation analyses were used to find an association between patient characteristics and HBL. Multivariate linear analysis was used to determine independent risk factors of HBL. Results: We reviewed 169 consecutive patients who underwent PLF surgery for degenerative spine in one institution. The mean amount of HBL was 588 mL, which was 39% of the total blood loss. On the basis of the model of multiple linear regression analysis, the multilevel fusion ( P =0.001), surgical time ( P =0.034), and fibrinogen level ( P =0.027) were independent risk factors that contributed to HBL, but age of 60 years or above ( P =0.110), postoperative complications ( P =0.278), and cell saver were not ( P =0.739). Conclusions: We conclude that a large amount of HBL may occur in patients who underwent PLF surgery for degenerative spine. In addition, significant hidden loss may have a correlation with postoperative mortality. Multilevel fused, surgical time, and fibrinogen level should be paid close attention when considering strategies of fluid infusion and blood transfusion.
    Type of Medium: Online Resource
    ISSN: 2380-0186
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2849652-8
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