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  • 1
    Online Resource
    Online Resource
    Fibroblast growth factor 18 attenuates liver fibrosis and HSCs activation via the SMO-LATS1-YAP pathway
    Elsevier BV ; 2022
    In:  Pharmacological Research Vol. 178 ( 2022-04), p. 106139-
    Details
    In: Pharmacological Research, Elsevier BV, Vol. 178 ( 2022-04), p. 106139-
    Type of Medium: Online Resource
    ISSN: 1043-6618
    URL: Article
    DOI: 10.1016/j.phrs.2022.106139
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1471456-5
    SSG: 15,3
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  • 2
    Online Resource
    Online Resource
    Omentin-1 attenuates glucocorticoid-induced cardiac injury by phosphorylating GSK3β
    Bioscientifica ; 2021
    In:  Journal of Molecular Endocrinology Vol. 66, No. 4 ( 2021-05-01), p. 273-283
    Details
    In: Journal of Molecular Endocrinology, Bioscientifica, Vol. 66, No. 4 ( 2021-05-01), p. 273-283
    Abstract: Glucocorticoid excess often causes a variety of cardiovascular complications, including hypertension, atherosclerosis, and cardiac hypertrophy. To abrogate its cardiac side effects, it is necessary to fully disclose the pathophysiological role of glucocorticoid in cardiac remodelling. Previous clinical and experimental studies have found that omentin-1, one of the adipokines, has beneficial effects in cardiovascular diseases, and is closely associated with metabolic disorders. However, there is no evidence to address the potential role of omentin-1 in glucocorticoid excess-induced cardiac injuries. To uncover the links, the present study utilized rat model with glucocorticoid-induced cardiac injuries and clinical patients with abnormal cardiac function. Chronic administration of glucocorticoid excess reduced rat serum omentin-1 concentration, which closely correlated with cardiac functional parameters. Intravenous administration of adeno-associated virus encoding omentin-1 upregulated the circulating omentin-1 level and attenuated glucocorticoid excess-induced cardiac hypertrophy and functional disorders. Overexpression of omentin-1 also improved cardiac mitochondrial function, including the reduction of lipid deposits, induction of mitochondrial biogenesis, and enhanced mitochondrial activities. Mechanistically, omentin-1 phosphorylated and activated the GSK3β pathway in the heart. From a study of 28 patients with Cushing’s syndrome and 23 healthy subjects, the plasma level of glucocorticoid was negatively correlated with omentin-1, and was positively associated with cardiac ejection fraction and fractional shortening. Collectively, the present study provided a novel role of omentin-1 in glucocorticoid excess-induced cardiac injuries and found that the omentin-1/GSK3β pathway was a potential therapeutic target in combating the side effects of glucocorticoid.
    Type of Medium: Online Resource
    ISSN: 0952-5041 , 1479-6813
    URL: Article
    DOI: 10.1530/JME-20-0236
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2021
    detail.hit.zdb_id: 1478171-2
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  • 3
    Online Resource
    Online Resource
    Determination and pharmacokinetic study of echinatin by UPLC-MS/MS in rat plasma
    Elsevier BV ; 2019
    In:  Journal of Pharmaceutical and Biomedical Analysis Vol. 168 ( 2019-05), p. 133-137
    Details
    In: Journal of Pharmaceutical and Biomedical Analysis, Elsevier BV, Vol. 168 ( 2019-05), p. 133-137
    Type of Medium: Online Resource
    ISSN: 0731-7085
    URL: Article
    DOI: 10.1016/j.jpba.2019.02.023
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 1491820-1
    SSG: 15,3
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  • 4
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    Online Resource
    The assessment of interhemispheric imbalance using functional near-infrared spectroscopic and transcranial magnetic stimulation for predicting motor outcome after stroke
    Frontiers Media SA ; 2023
    In:  Frontiers in Neuroscience Vol. 17 ( 2023-8-16)
    Details
    In: Frontiers in Neuroscience, Frontiers Media SA, Vol. 17 ( 2023-8-16)
    Abstract: To investigate changes in interhemispheric imbalance of cortical excitability during motor recovery after stroke and to clarify the relationship between motor function recovery and alterations in interhemispheric imbalance, with the aim to establish more effective neuromodulation strategies. Methods Thirty-one patients underwent assessments of resting motor threshold (RMT) using transcranial magnetic stimulation (TMS); the cortical activity of the primary motor cortex (M1), premotor cortex (PMC), and supplementary motor area (SMA) using functional near-infrared spectroscopy (fNIRS); as well as motor function using upper extremity Fugl-Meyer (FMA-UE). The laterality index (LI) of RMT and fNIRS were also calculated. All indicators were measured at baseline(T 1 ) and 1 month later(T 2 ). Correlations between motor function outcome and TMS and fNIRS metrics at baseline were analyzed using bivariate correlation. Results All the motor function (FMA-UE 1 , FMA-UE 2 , FMA-d 2 ) and LI-RMT (LI-RMT 1 and LI-RMT 2 ) had a moderate negative correlation. The higher the corticospinal excitability of the affected hemisphere, the better the motor outcome of the upper extremity, especially in the distal upper extremity ( r  = −0.366, p  = 0.043; r  = −0.393, p  = 0.029). The greater the activation of the SMA of the unaffected hemisphere, the better the motor outcome, especially in the distal upper extremity ( r  = −0.356, p  = 0.049; r  = −0.367, p  = 0.042). There was a significant moderate positive correlation observed between LI-RMT 2 and LI-SMA 1 ( r  = 0.422, p  = 0.018). The improvement in motor function was most significant when both LI-RMT 1 and LI-SMA 1 were lower. Besides, in patients dominated by unaffected hemisphere corticospinal excitability during motor recovery, LI-(M1 + SMA + PMC) 2 exhibited a significant moderate positive association with the proximal upper extremity function 1 month later ( r  = 0.642, p  = 0.007). Conclusion The combination of both TMS and fNIRS can infer the prognosis of motor function to some extent. Which can infer the role of both hemispheres in recovery and may contribute to the development of effective individualized neuromodulation strategies.
    Type of Medium: Online Resource
    ISSN: 1662-453X
    URL: Article
    DOI: 10.3389/fnins.2023.1231693
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2411902-7
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  • 5
    Online Resource
    Online Resource
    Table_1.docx
    Frontiers Media SA ; 2021
    In:  Frontiers in Oncology Vol. 10 ( 2021-2-1)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 10 ( 2021-2-1)
    Abstract: ST3Gal IV is one of the principal sialyltransferases responsible for the biosynthesis of α2, 3-sialic acid to the termini N -glycans or O- glycans of glycoproteins and glycolipids. It has been reported that ST3Gal IV expression is associated with gastric carcinoma, pancreatic adenocarcinoma and breast cancer. While the expression and functions of ST3Gal IV in cervical cancer are still poorly understood. In this study, we found that ST3Gal IV was downregulated in human cervical cancer tissues compared to normal cervix tissues, and ST3Gal IV expression was negatively associated with the pathological grade of cervical cancer. ST3Gal IV upregulation inhibited the growth and proliferation of cervical cancer HeLa and SiHa cells in vitro and in vivo . Furthermore, ST3Gal IV overexpression enhanced the expression of several Notch pathway components such as Jagged1, Notch1, Hes1 and Hey1, while cell cycle protein expression like Cyclin D1, Cyclin E1, CDK2 and CDK4 were decreased. These results indicate that expression of ST3Gal IV is reduced in cervical cancer and plays a negative role in cell proliferation via Notch/p21/CDKs signaling pathway. Thus, sialyltransferase ST3Gal IV might be a target for the diagnosis and therapy of cervical cancer.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2020.540332
    DOI: 10.3389/fonc.2020.540332.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2649216-7
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  • 6
    Online Resource
    Online Resource
    Aerobic Exercise Improves Type 2 Diabetes Mellitus-Related Cognitive Impairment by Inhibiting JAK2/STAT3 and Enhancing AMPK/SIRT1 Pathways in Mice
    Hindawi Limited ; 2022
    In:  Disease Markers Vol. 2022 ( 2022-5-5), p. 1-15
    Details
    In: Disease Markers, Hindawi Limited, Vol. 2022 ( 2022-5-5), p. 1-15
    Abstract: Type 2 diabetes mellitus (T2DM) is a prevalent risk factor for cognitive impairment. Aerobic exercise can improve T2DM-related cognitive impairment; however, the possible mechanisms remain elusive. Thus, we assessed db/m mice and leptin receptor-deficient (db/db) mice that did or did not perform aerobic exercise (8 m/min, 60 min/day, and 5 days/week for 12 weeks). In this study, cognitive function was significantly impaired in the T2DM mice; aerobic exercise improved cognitive impairment through activating the AMPK/SIRT1 signalling pathway and inhibiting the JAK2/STAT3 signalling pathway in T2DM mice. However, after the application of RO8191 (JAK2 activator) or Compound C (AMPK inhibitor), the positive improvement of the exercise was evidently suppressed. Taken together, our data indicated that long-term aerobic exercise improves type 2 diabetes mellitus-related cognitive impairment by inhibiting JAK2/STAT3 and enhancing AMPK/SIRT1 pathways in mice.
    Type of Medium: Online Resource
    ISSN: 1875-8630 , 0278-0240
    URL: Article
    DOI: 10.1155/2022/6010504
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2033253-1
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  • 7
    Online Resource
    Online Resource
    Single-cell sequencing deciphers a convergent evolution of copy number alterations from primary to circulating tumor cells
    Cold Spring Harbor Laboratory ; 2017
    In:  Genome Research Vol. 27, No. 8 ( 2017-08), p. 1312-1322
    Details
    In: Genome Research, Cold Spring Harbor Laboratory, Vol. 27, No. 8 ( 2017-08), p. 1312-1322
    Abstract: Copy number alteration (CNA) is a major contributor to genome instability, a hallmark of cancer. Here, we studied genomic alterations in single primary tumor cells and circulating tumor cells (CTCs) from the same patient. Single-nucleotide variants (SNVs) in single cells from both samples occurred sporadically, whereas CNAs among primary tumor cells emerged accumulatively rather than abruptly, converging toward the CNA in CTCs. Focal CNAs affecting the MYC gene and the PTEN gene were observed only in a minor portion of primary tumor cells but were present in all CTCs, suggesting a strong selection toward metastasis. Single-cell structural variant (SV) analyses revealed a two-step mechanism, a complex rearrangement followed by gene amplification, for the simultaneous formation of anomalous CNAs in multiple chromosome regions. Integrative CNA analyses of 97 CTCs from 23 patients confirmed the convergence of CNAs and revealed single, concurrent, and mutually exclusive CNAs that could be the driving events in cancer metastasis.
    Type of Medium: Online Resource
    ISSN: 1088-9051 , 1549-5469
    URL: Article
    DOI: 10.1101/gr.216788.116
    RVK:
    XA 10000
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2017
    detail.hit.zdb_id: 1483456-X
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Data_Sheet_1.pdf
    Frontiers Media SA ; 2023
    In:  Frontiers in Neurology Vol. 14 ( 2023-5-18)
    Details
    In: Frontiers in Neurology, Frontiers Media SA, Vol. 14 ( 2023-5-18)
    Abstract: Hereditary spastic paraplegia (HSP) is a heterogeneous group of inherited neurodegenerative disorders that currently have no cure. HSP type 11 (SPG11-HSP) is a complex form carrying mutations in the SPG11 gene. Neuropathological studies demonstrate that motor deficits in these patients are mainly attributed to axonal degeneration of the corticospinal tract (CST). Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive technique that can induce central nervous system plasticity and promote neurological recovery by modulating the excitability of cortical neuronal cells. Although rTMS is expected to be a therapeutic tool for neurodegenerative diseases, no previous studies have applied rTMS to treat motor symptoms in SPG11-HSP. Here, we report a case of SPG11-HSP with lower extremity spasticity and gait instability, which were improved by applying high-frequency rTMS (HF-rTMS) at the primary motor cortex (M1). Clinical and physiological features were measured throughout the treatment, including the Modified Ashworth Scale (MAS), Berg Balance Scale (BBS), the timed up and go (TUG) test and the 10-meter walk test time (10 MWT). The structure and excitability of the CST were assessed by diffusion tensor imaging (DTI) and transcranial magnetic stimulation (TMS), respectively. After treatment, the patient gained 17 points of BBS, along with a gradual decrease in MAS scores of the bilateral lower extremity. In addition, the TUG test and 10 MWT improved to varying degrees. TMS assessment showed increased motor evoked potential (MEP) amplitude, decreased resting motor threshold (RMT), decreased central motor conduction time (CMCT), and decreased difference in the cortical silent period (CSP) between bilateral hemispheres. Using the DTI technique, we observed increased fractional anisotropy (FA) values and decreased mean diffusivity (MD) and radial diffusivity (RD) values in the CST. It suggests that applying HF-rTMS over the bilateral leg area of M1 (M1-LEG) is beneficial for SPG11-HSP. In this study, we demonstrate the potential of rTMS to promote neurological recovery from both functional and structural perspectives. It may provide a clinical rationale for using rTMS in the rehabilitation of HSP patients.
    Type of Medium: Online Resource
    ISSN: 1664-2295
    URL: Article
    URL: Article
    DOI: 10.3389/fneur.2023.1162149
    DOI: 10.3389/fneur.2023.1162149.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2564214-5
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