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  • Ovid Technologies (Wolters Kluwer Health)  (6)
  • Zhang, Jingjing  (6)
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  • Ovid Technologies (Wolters Kluwer Health)  (6)
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  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Medicine Vol. 97, No. 32 ( 2018-08), p. e11685-
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 32 ( 2018-08), p. e11685-
    Type of Medium: Online Resource
    ISSN: 0025-7974
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 80184-7
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  • 2
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. suppl_1 ( 2013-02)
    Abstract: Background: Neural cell apoptosis is one of the dominated mechanisms of cerebral ischemia-reperfusion injury (IRI). Anti-apotosis factor Mcl1 and apotosis factor p53 have been confirmed to play crucial roles in the apoptotic regulation previously. Mcl1 and p53 are the substrates of the ubiquitin ligases Huwe1, and which has been suggested as a potent therapeutic target in regulating cell apoptosis. Our aim is to explore whether Huwe1 modulates neural apoptosis by degrading Mcl1, p53 in cerebral ischemia-reperfusion injury. Methods: Eight health male adult rhesus monkeys were recruited in our study and were randomly devided into four groups: sham, PBS, siRNA silencing Huwe1 lentiviral vector and empty vector group. Except the sham group, the other groups were received corespondant intracranial injections and transient right middle cerebral occlusion (MCAO). A series of neurological evaluation and MRI were ulitized to evaluate animals. GFP flurescence was used to test transfection efficiency and apoptosis was detected by TUNEL staining. The expression level of related factors in causatum, putamen, temporal lobe and hippocampus were analyzed with western blot, QPCR, and immunohistochemistry. Results: The neurological deficit was much more serious in the silencing Huwe1 group than both empty vector and PBS group. The expression of Huwe1, Mcl1 and P53 were appeared a tendency to upregulate in the right caudatum and putament in model group than sham group in both protein and nucleotides level. Moreover, the number of apoptosis cells tested by TUNEL was the highest in the silencing Huwe 1 group, induced by decreasing expression of Huwe1 and obviously upragulating P53 expression. However, none of them has significant difference in other remote positions. Conclusion: Our study provides a potential novel mechnism that Huwe1 palys an important role in regulating neural apoptosis by regadading Mcl1 and P53 in cerebral IRI. In addition, for the first time, we confirm that the anti-apoptosis factor Mcl1 engages in the pathogenesis of cerebral IRI. It is possible that Huwe1 can be a potential therapeutic target for cerebral ischemia.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 80381-9
    detail.hit.zdb_id: 1467823-8
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  • 3
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Critical Care Medicine Vol. 46, No. 12 ( 2018-12), p. e1167-e1174
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 12 ( 2018-12), p. e1167-e1174
    Abstract: The purpose of this study was to investigate the association between mean arterial pressure fluctuations and mortality in critically ill patients admitted to the ICU. Design: Retrospective cohort. Setting: All adult ICUs at a tertiary care hospital. Patients: All adult patients with complete mean arterial pressure records were selected for analysis in the Multiparameter Intelligent Monitoring in Intensive Care II database. Patients in the external cohort were newly recruited adult patients in the Medical Information Mart for Intensive Care III database. Interventions: None. Measurements and Main Results: The records of 8,242 patients were extracted. Mean arterial pressure fluctuation was calculated as follows: (mean nighttime mean arterial pressure – mean daytime mean arterial pressure)/mean arterial pressure. Patients were divided into two groups according to the degree of mean arterial pressure fluctuation: group A (between –5% and 5%) and group B ( 〈 –5% and 〉 5%). The endpoints of this study were ICU and hospital mortality. Patients in group A ( n = 4,793) had higher ICU and hospital mortality than those in group B ( n = 3,449; 11.1% vs 8.1%, p 〈 0.001 and 13.8% vs 10.1%, p 〈 0.001, respectively). After adjusting for other covariates, the mean arterial pressure fluctuations between –5% and 5% were significantly correlated with ICU mortality (odds ratio, 1.296; 95% CI, 1.103–1.521; p = 0.002) and hospital mortality (odds ratio, 1.323; 95% CI, 1.142–1.531; p 〈 0.001). This relationship remained remarkable in patients with low or high Sequential Organ Failure Assessment scores in the sensitive analysis. Furthermore, external validation on a total of 4,502 individuals revealed that patients in group A still had significantly higher ICU ( p 〈 0.001) and hospital mortality ( p 〈 0.001) than those in group B. Conclusions: The reduced mean arterial pressure fluctuation (within –5% and 5%) may be associated with ICU and hospital mortality in critically ill patients.
    Type of Medium: Online Resource
    ISSN: 0090-3493
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 197890-1
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  • 4
    In: Clinical Nuclear Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 48, No. 10 ( 2023-10), p. 861-868
    Abstract: This head-to-head comparison study was designed to investigate the radiotracer uptake and clinical feasibility of using 68 Ga-LNC1007, to detect the primary and metastatic lesions in patients with various types of cancer, and to compare the results with those of 2- 18 F-FDG PET/CT and 68 Ga-FAPI-02 PET/CT. Patients and Methods Sixty-one patients with 10 different kinds of cancers were enrolled in this study. Among them, 50 patients underwent paired 68 Ga-LNC1007 and 2- 18 F-FDG PET/CT, and the other 11 patients underwent paired 68 Ga-LNC1007 and 68 Ga-FAPI-02 PET/CT. The final diagnosis was based on histopathological results and diagnostic radiology. Immunohistochemistry for FAP and integrin α v β 3 was performed in 24 primary tumors. Results 68 Ga-LNC1007 PET/CT detected all 55 primary tumors, whereas 2- 18 F-FDG PET/CT was visually positive for 45 primary tumors ( P = 0.002). Furthermore, subgroup analysis showed that 68 Ga-LNC1007 PET/CT was superior to 2- 18 F-FDG PET/CT in diagnosing renal cell carcinomas and hepatocellular carcinomas. For metastatic tumors, 68 Ga-LNC1007 PET/CT revealed more PET-positive lesions and higher SUV max for skeletal metastases and peritoneal metastases compared with 2- 18 F-FDG. The SUV max and tumor-to-background ratio of primary tumors on 68 Ga-LNC1007 PET/CT were much higher than those on 68 Ga-FAPI-02 PET/CT, the same was also observed for metastatic tumors. Immunohistochemical results showed that the SUV mean quantified from 68 Ga-LNC1007 PET was correlated with FAP expression level ( r = 0.564, P = 0.005). Conclusions 68 Ga-LNC1007 is a promising new diagnostic PET tracer for imaging of various kinds of malignant lesions. It may be a better alternative to 2- 18 F-FDG for diagnosing renal cell carcinoma, hepatocellular carcinoma, skeletal metastases, and peritoneal metastases.
    Type of Medium: Online Resource
    ISSN: 1536-0229 , 0363-9762
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2045053-9
    detail.hit.zdb_id: 197628-X
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Blood Pressure Monitoring Vol. 22, No. 4 ( 2017-08), p. 191-195
    In: Blood Pressure Monitoring, Ovid Technologies (Wolters Kluwer Health), Vol. 22, No. 4 ( 2017-08), p. 191-195
    Type of Medium: Online Resource
    ISSN: 1359-5237
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 1324472-3
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  • 6
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 47, No. suppl_1 ( 2016-02)
    Abstract: Background and purpose: The proteasome subunit α type 6 (PSMA6) is an important proteolytic protein regulating the expression of genes involved in inflammation. Recently, a functional polymorphism rs1048990, located in PSMA6 , has been reported with the susceptibility to ischemic stroke (IS) in several ethnic cohorts, but the results were inconsistent. Moreover, it still lacks the data in Asian. The purpose of the present study was to determine whether this polymorphism confers significant risk to IS in a Chinese population. Methods: A total of 1102 IS cases and 975 healthy controls were analyzed in our study. We genotyped rs1048990 with ligation detection reaction (LDR) method and then performed a meta-analysis. Results: Significant association between rs1048990 in PSMA6 and ischemic stroke was observed in all comparison models (genotype, p =0.016; allele, p =0.004; CG+GG vs. CC, adjusted p =0.006; GG vs. CG+CC, adjusted p =0.038). Further stratification for stroke subtype, similar differences also can be found in large artery atherosclerosis and cardioembolism, but not small vessel occlusion. In addition, in the analysis of genotype-phenotype correlation, the onset ages of allele-G carriers have a trend to be older than non-carriers’ ( p 〈 0.001). In the meta-analysis, there is no significant difference between rs1048990 and ischemic stroke, for the great discrepancy of the genotype composition between Caucasian and Chinese. Conclusion: Our study suggests that rs1048990 contributes to the risk of IS and its subtypes in Chinese population, but these associations may vary in different ethnic populations.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 80381-9
    detail.hit.zdb_id: 1467823-8
    Location Call Number Limitation Availability
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