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- Shen, JL, et al.
(författare)
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Cervical vestibular evoked myogenic potentials in 3-month-old infants: Comparative characteristics and feasibility for infant vestibular screening
- 2022
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Ingår i: Frontiers in neurology. - : Frontiers Media SA. - 1664-2295. ; 13, s. 992392-
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Tidskriftsartikel (refereegranskat)abstract
- We compared the characteristics of air-conducted sound cervical vestibular evoked myogenic potential (ACS-cVEMP) and bone-conducted vibration cVEMP (BCV-cVEMP) among 3-month-old infants with normal hearing and sensorineural hearing loss (SNHL), and healthy adults to explore the feasibility and optimal strategies for infant vestibular screening.Methods29 infants (58 ears) were divided into two groups according to hearing (group I: normal hearing ears; group II: SNHL ears), 20 healthy adults were defined as group III. The results of response rate, P13 and N23 latency, P13-N23 interval, amplitudes, and corrected interaural asymmetry ratio (IAR) were recorded and compared among three groups.ResultsThe response rates of ACS-cVEMP in three groups were 88.89, 62.00, 100%, respectively. The P13 and N23 latencies, and P13-N23 interval did not differ significantly between group I and II (p = 0.866, p = 0.190, p = 0.252). A significant difference was found between group I and III (p = 0.016, p < 0.001, p < 0.001). No significant difference was observed in raw or corrected amplitude between group I and II (p = 0.741, p = 0.525), while raw and corrected amplitudes in group III were significantly larger than group I (p < 0.001, p < 0.001). For BCV-cVEMP, the response rates in three groups were 100, 86.36, 100%, respectively, No significant difference existed in the P13 and N23 latency, or P13-N23 interval between group I and II (p = 0.665, p = 0.925, p = 0.806), however, P13 and N23 latencies were significantly longer in group III than group I (p < 0.001, p = 0.018), but not in P13-N23 interval (p = 0.110). There was no significant difference in raw or corrected amplitude between group I and II (p = 0.771, p = 0.155) or in raw amplitude between group I and III (p = 0.093), however, a significant difference existed in corrected amplitude between group I and III (p < 0.001).ConclusionsCompared with adults, 3-month-old infants with normal hearing presented with equivalent response rates, shorter P13 and N23 latencies, smaller corrected amplitudes, and a wider IAR range for both ACS and BCV-cVEMP. SNHL infants had equivalent response rates of BCV-cVEMP, lower response rates of ACS-cVEMP than normal hearing infants. When responses were present, characteristics of ACS and BCV-cVEMP in SNHL infants were similar with normal hearing infants. ACS combined with BCV-cVEMP are recommended to improve the accuracy of vestibular screening.
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- Wu, ZC, et al.
(författare)
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Tumor suppressor ZHX2 inhibits NAFLD-HCC progression via blocking LPL-mediated lipid uptake
- 2020
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Ingår i: Cell death and differentiation. - : Springer Science and Business Media LLC. - 1476-5403 .- 1350-9047. ; 27:5, s. 1693-1708
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Tidskriftsartikel (refereegranskat)abstract
- Non-alcoholic fatty liver disease (NAFLD) leads to hepatocellular carcinoma (HCC). However, the underlying mechanism remains largely unclear. Here, we investigated the role of the tumor suppressor Zinc fingers and homeoboxes 2 (ZHX2) in the progression of NAFLD to HCC. ZHX2 expression was significantly decreased in fatty liver tissues, especially in the liver with NAFLD–HCC. ZHX2 overexpression disturbed lipid homeostasis of cultured HCC cells, and inhibited lipid deposition in hepatocytes both in vitro and in vivo. Moreover, ZHX2 inhibited uptake of exogenous lipids through transcriptional suppression of lipid lipase (LPL), leading to retarded proliferation of HCC cells. Importantly, LPL overexpression significantly reversed ZHX2-mediated inhibition of HCC cell proliferation, xenograft tumor growth, lipid deposition, and spontaneous liver tumor formation. Consistently, IHC staining demonstrated a negative correlation of ZHX2 with LPL in an HCC cohort. Collectively, ZHX2 protects hepatocytes from abnormal lipid deposition in NAFLD through transcriptional repression of LPL, which subsequently retards cell growth and NAFLD–HCC progression. These findings illustrate a novel mechanism of NAFLD progression into HCC.
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- Zhou, ZC, et al.
(författare)
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Downregulation of Erythrocyte miR-210 Induces Endothelial Dysfunction in Type 2 Diabetes
- 2022
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 71:2, s. 285-297
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Tidskriftsartikel (refereegranskat)abstract
- Red blood cells (RBC) act as mediators of vascular injury in type 2 diabetes mellitus (T2DM). miR-210 plays a protective role in cardiovascular homeostasis and is decreased in whole blood of T2DM mice. We hypothesized that downregulation of RBC miR-210 induces endothelial dysfunction in T2DM. RBC were coincubated with arteries and endothelial cells ex vivo and transfused in vivo to identify the role of miR-210 and its target protein tyrosine phosphatase 1B (PTP1B) in endothelial dysfunction. RBC from patients with T2DM and diabetic rodents induced endothelial dysfunction ex vivo and in vivo. miR-210 levels were lower in human RBC from patients with T2DM (T2DM RBC) than in RBC from healthy subjects. Transfection of miR-210 in human T2DM RBC rescued endothelial function, whereas miR-210 inhibition in healthy subjects RBC or RBC from miR-210 knockout mice impaired endothelial function. Human T2DM RBC decreased miR-210 expression in endothelial cells. miR-210 expression in carotid artery plaques was lower in T2DM patients than in patients without diabetes. Endothelial dysfunction induced by downregulated RBC miR-210 involved PTP1B and reactive oxygen species. miR-210 mimic attenuated endothelial dysfunction induced by RBC via downregulating vascular PTP1B and oxidative stress in diabetic mice in vivo. These data reveal that the downregulation of RBC miR-210 is a novel mechanism driving the development of endothelial dysfunction in T2DM.
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