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  • Ovid Technologies (Wolters Kluwer Health)  (4)
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  • Ovid Technologies (Wolters Kluwer Health)  (4)
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  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Medicine Vol. 102, No. 7 ( 2023-02-17), p. e32935-
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 7 ( 2023-02-17), p. e32935-
    Abstract: Unintended pregnancy is a problem that women encounter throughout their reproductive age. Excessive and prolonged uterine bleeding is one of the most common and critical adverse reactions of induced abortion, for it increases the risk of anemia and intrauterine infection. To provide reliable clinical evidence, we performed a protocol for systematic review and meta-analysis to evaluate the hemostatic effect of motherwort in postabortion. Methods: This review protocol has been registered in the international prospective register of systematic reviews. The statement of Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols will be used as guidelines for reporting present review protocol. Original clinical randomized controlled trials assessing the beneficial effects and safety of motherwort on induced abortion will be included. Databases searched include China National Knowledge Infrastructure, Chinese Scientific Journals Database, Wanfang Database, China Biological Medicine Database, PubMed, and EMBASE Database and Cochrane Central Register of Controlled Trials. Cochrane collaboration tool is used to assess the risk of bias of included randomized controlled trials. All calculations are carried out with Stata 11.0 (The Cochrane Collaboration, Oxford, United Kingdom). Results: This systematic review and meta-analysis will provide a detailed summary of the current evidence related to the efficacy of motherwort injection preventing postabortion hemorrhage after induced abortion. Conclusion: This evidence will be useful to practitioners, patients, and health policy-makers regarding the use of motherwort injection in induced abortion.
    Type of Medium: Online Resource
    ISSN: 0025-7974
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2049818-4
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  • 2
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 21 ( 2021-05-28), p. e26143-
    Abstract: Coronavirus disease 2019 (COVID-19) is a rapidly emerging infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2. Currently, more than 100 million cases of COVID-19 have been confirmed worldwide, with over 2.4 million mortalities. The pandemic affects people of all ages but older individuals and those with severe chronic illnesses, including cancer patients, are at higher risk. Patient concerns: The impact of cancer treatment on the progression of COVID-19 is unclear. Therefore, we assessed the effects of chemotherapy on COVID-19 outcomes for 2 cancer patients. On January 24, 2020, a level I response to a major public health emergency was initiated in Hubei Province, China, which includes Enshi Autonomous Prefecture that has a population of 4.026 million people. As of April 30, 2020, 252 confirmed cases of COVID-19 and 11 asymptomatic carriers were identified in Enshi. Diagnosis: Among the confirmed cases and asymptomatic carriers, 2 patients were identified who were previously diagnosed with malignant tumors, including one with hepatocellular carcinoma and the other with cardia carcinoma. Interventions: These 2 patients were receiving or just completed chemotherapy at the time of their COVID-19 diagnosis. Outcomes: Both patients were followed and presented favorable outcomes. The positive outcomes for these 2 patients could be partially explained by their recent chemotherapy that impacted their immune status. Also, their relatively younger ages and lack of comorbidities were likely factors in their successful recovery from COVID-19. Conclusions: Anticancer treatment might enhance a patient's ability to respond favorably to COVID-19 infection. However, anticancer treatment is likely to impact immune function differently in different individuals, which can influence disease outcomes.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049818-4
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  • 3
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. 2 ( 2023-01-20), p. 208-222
    Abstract: ASPP1 (apoptosis stimulating of p53 protein 1) is critical in regulating cell apoptosis as a cofactor of p53 to promote its transcriptional activity in the nucleus. However, whether cytoplasmic ASPP1 affects p53 nuclear trafficking and its role in cardiac diseases remains unknown. This study aims to explore the mechanism by which ASPP1 modulates p53 nuclear trafficking and the subsequent contribution to cardiac ischemia/reperfusion (I/R) injury. Methods and Results: The immunofluorescent staining showed that under normal condition ASPP1 and p53 colocalized in the cytoplasm of neonatal mouse ventricular cardiomyocytes, while they were both upregulated and translocated to the nuclei upon hypoxia/reoxygenation treatment. The nuclear translocation of ASPP1 and p53 was interdependent, as knockdown of either ASPP1 or p53 attenuated nuclear translocation of the other one. Inhibition of importin-β1 resulted in the cytoplasmic sequestration of both p53 and ASPP1 in neonatal mouse ventricular cardiomyocytes with hypoxia/reoxygenation stimulation. Overexpression of ASPP1 potentiated, whereas knockdown of ASPP1 inhibited the expression of Bax (Bcl2-associated X), PUMA (p53 upregulated modulator of apoptosis), and Noxa, direct apoptosis-associated targets of p53. ASPP1 was also increased in the I/R myocardium. Cardiomyocyte-specific transgenic overexpression of ASPP1 aggravated I/R injury as indicated by increased infarct size and impaired cardiac function. Conversely, knockout of ASPP1 mitigated cardiac I/R injury. The same qualitative data were observed in neonatal mouse ventricular cardiomyocytes exposed to hypoxia/reoxygenation injury. Furthermore, inhibition of p53 significantly blunted the proapoptotic activity and detrimental effects of ASPP1 both in vitro and in vivo. Conclusions: Binding of ASPP1 to p53 triggers their nuclear cotranslocation via importin-β1 that eventually exacerbates cardiac I/R injury. The findings imply that interfering the expression of ASPP1 or the interaction between ASPP1 and p53 to block their nuclear trafficking represents an important therapeutic strategy for cardiac I/R injury.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1467838-X
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Hepatology Vol. 74, No. 3 ( 2021-09), p. 1319-1338
    In: Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 74, No. 3 ( 2021-09), p. 1319-1338
    Abstract: NAFLD has become the most common liver disease worldwide but lacks a well‐established pharmacological therapy. Here, we aimed to investigate the role of an E3 ligase SH3 domain‐containing ring finger 2 (SH3RF2) in NAFLD and to further explore the underlying mechanisms. Methods and Results In this study, we found that SH3RF2 was suppressed in the setting of NAFLD across mice, monkeys, and clinical individuals. Based on a genetic interruption model, we further demonstrated that hepatocyte SH3RF2 deficiency markedly deteriorates lipid accumulation in cultured hepatocytes and diet‐induced NAFLD mice. Mechanistically, SH3RF2 directly binds to ATP citrate lyase, the primary enzyme promoting cytosolic acetyl–coenzyme A production, and promotes its K48‐linked ubiquitination‐dependent degradation. Consistently, acetyl–coenzyme A was significantly accumulated in Sh3rf2 ‐knockout hepatocytes and livers compared with wild‐type controls, leading to enhanced de novo lipogenesis, cholesterol production, and resultant lipid deposition. Conclusion SH3RF2 depletion in hepatocytes is a critical aggravator for NAFLD progression and therefore represents a promising therapeutic target for related liver diseases.
    Type of Medium: Online Resource
    ISSN: 0270-9139 , 1527-3350
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1472120-X
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