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  • 1
    Online Resource
    Online Resource
    Heart-Ankle Pulse Wave Velocity Is Superior to Brachial-Ankle Pulse Wave Velocity in Detecting Aldosterone-Induced Arterial Stiffness
    MDPI AG ; 2021
    In:  Biomedicines Vol. 9, No. 10 ( 2021-09-22), p. 1285-
    Details
    In: Biomedicines, MDPI AG, Vol. 9, No. 10 ( 2021-09-22), p. 1285-
    Abstract: Primary aldosteronism (PA) is associated with higher arterial stiffness compared to essential hypertension (EH). However, few studies have compared different pulse wave velocity (PWV) parameters to detect aldosterone-induced arterial stiffness. In this study, we aimed to compare the sensitivity in detecting aldosterone-induced arterial stiffness between brachial-ankle PWV (baPWV) and heart-ankle PWV (haPWV). We prospectively enrolled 1006 PA patients and 983 EH patients. Detailed medical history, basic biochemistry data and two PWV measurements (baPWV and haPWV) were collected in both groups. We performed analysis on the original cohort and two propensity score matching (PSM) models (model 1 adjusted for age and sex; model 2 adjusted for age, sex, systolic and diastolic blood pressure). The DeLong test was used to compare areas under receiver operating characteristic curves (AUCs) between baPWV and haPWV to predict PA. In all models, the PA patients had significantly higher baPWV compared to the EH patients. The AUC of haPWV was greater than that of baPWV. In conclusion, haPWV seems to be a better PWV parameter than baPWV in detecting aldosterone-induced arterial stiffness.
    Type of Medium: Online Resource
    ISSN: 2227-9059
    URL: Article
    DOI: 10.3390/biomedicines9101285
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2720867-9
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  • 2
    Online Resource
    Online Resource
    Lipids and Lipoproteins in Health and Disease: Focus on Targeting Atherosclerosis
    MDPI AG ; 2021
    In:  Biomedicines Vol. 9, No. 8 ( 2021-08-09), p. 985-
    Details
    In: Biomedicines, MDPI AG, Vol. 9, No. 8 ( 2021-08-09), p. 985-
    Abstract: Despite advances in pharmacotherapy, intervention devices and techniques, residual cardiovascular risks still cause a large burden on public health. Whilst most guidelines encourage achieving target levels of specific lipids and lipoproteins to reduce these risks, increasing evidence has shown that molecular modification of these lipoproteins also has a critical impact on their atherogenicity. Modification of low-density lipoprotein (LDL) by oxidation, glycation, peroxidation, apolipoprotein C-III adhesion, and the small dense subtype largely augment its atherogenicity. Post-translational modification by oxidation, carbamylation, glycation, and imbalance of molecular components can reduce the capacity of high-density lipoprotein (HDL) for reverse cholesterol transport. Elevated levels of triglycerides (TGs), apolipoprotein C-III and lipoprotein(a), and a decreased level of apolipoprotein A-I are closely associated with atherosclerotic cardiovascular disease. Pharmacotherapies aimed at reducing TGs, lipoprotein(a), and apolipoprotein C-III, and enhancing apolipoprotein A-1 are undergoing trials, and promising preliminary results have been reported. In this review, we aim to update the evidence on modifications of major lipid and lipoprotein components, including LDL, HDL, TG, apolipoprotein, and lipoprotein(a). We also discuss examples of translating findings from basic research to potential therapeutic targets for drug development.
    Type of Medium: Online Resource
    ISSN: 2227-9059
    URL: Article
    DOI: 10.3390/biomedicines9080985
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2720867-9
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  • 3
    Online Resource
    Online Resource
    KCNJ5 Somatic Mutations in Aldosterone-Producing Adenoma Are Associated with a Greater Recovery of Arterial Stiffness
    MDPI AG ; 2021
    In:  Cancers Vol. 13, No. 17 ( 2021-08-26), p. 4313-
    Details
    In: Cancers, MDPI AG, Vol. 13, No. 17 ( 2021-08-26), p. 4313-
    Abstract: Primary aldosteronism is the most common form of secondary hypertension and induces various cardiovascular injuries. In aldosterone-producing adenoma (APA), the impact of KCNJ5 somatic mutations on arterial stiffness excluding the influence of confounding factors is uncertain. We enrolled 213 APA patients who were scheduled to undergo adrenalectomy. KCNJ5 gene sequencing of APA was performed. After propensity score matching (PSM) for age, sex, body mass index, blood pressure, number of hypertensive medications, and hypertension duration, there were 66 patients in each group with and without KCNJ5 mutations. The mutation carriers had a higher aldosterone level and lower log transformed brachial–ankle pulse wave velocity (baPWV) than the non-carriers before PSM, but no difference in log baPWV after PSM. One year after adrenalectomy, the mutation carriers had greater decreases in log plasma aldosterone concentration, log aldosterone–renin activity ratio, and log baPWV than the non-carriers after PSM. Only the mutation carriers had a significant decrease in log baPWV after surgery both before and after PSM. KCNJ5 mutations were not correlated with baseline baPWV after PSM but were significantly correlated with ∆baPWV after surgery both before and after PSM. Conclusively, APA patients with KCNJ5 mutations had a greater regression in arterial stiffness after adrenalectomy than those without mutations.
    Type of Medium: Online Resource
    ISSN: 2072-6694
    URL: Article
    DOI: 10.3390/cancers13174313
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2527080-1
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  • 4
    Online Resource
    Online Resource
    Aldosterone Suppresses Endothelial Mitochondria through Mineralocorticoid Receptor/Mitochondrial Reactive Oxygen Species Pathway
    MDPI AG ; 2022
    In:  Biomedicines Vol. 10, No. 5 ( 2022-05-12), p. 1119-
    Details
    In: Biomedicines, MDPI AG, Vol. 10, No. 5 ( 2022-05-12), p. 1119-
    Abstract: Excessive aldosterone secretion causes endothelial dysfunction, vascular inflammation, and vascular fibrosis in patients with primary aldosteronism (PA). Endothelial function is closely related to endothelial mitochondria. However, the effects of elevated aldosterone levels on endothelial mitochondria remain unclear. In this study, we used primary cultured human umbilical vein endothelial cells (HUVECs) to investigate the effects of aldosterone on endothelial mitochondria. Mineralocorticoid receptor (MR) small interfering (si)RNA or glucocorticoid receptor (GR) siRNA were used to confirm the pathway by which aldosterone exerts its effects on the mitochondria of HUVECs. The results showed that excess aldosterone suppressed mitochondrial DNA copy numbers, anti-mitochondrial protein, and SOD2 protein expression in a dose- and time-dependent manner. These effects were attenuated by treatment with MR siRNA, but not with GR siRNA. Furthermore, it was attenuated by treatment with a mitochondria-targeted antioxidant (Mito-TEMPO, associated with mitochondrial reactive oxygen species (ROS) production), but not N-acetyl-L-cysteine (associated with cytosolic ROS production), which suggests that the process was through the mitochondrial ROS pathway, but not the cytosolic ROS pathway. In conclusion, aldosterone excess suppressed endothelial mitochondria through the MR/mitochondrial ROS pathway.
    Type of Medium: Online Resource
    ISSN: 2227-9059
    URL: Article
    DOI: 10.3390/biomedicines10051119
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2720867-9
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  • 5
    Online Resource
    Online Resource
    Endothelial Dysfunction in Primary Aldosteronism
    MDPI AG ; 2019
    In:  International Journal of Molecular Sciences Vol. 20, No. 20 ( 2019-10-21), p. 5214-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 20, No. 20 ( 2019-10-21), p. 5214-
    Abstract: Primary aldosteronism (PA) is characterized by excess production of aldosterone from the adrenal glands and is the most common and treatable cause of secondary hypertension. Aldosterone is a mineralocorticoid hormone that participates in the regulation of electrolyte balance, blood pressure, and tissue remodeling. The excess of aldosterone caused by PA results in an increase in cardiovascular and cerebrovascular complications, including coronary artery disease, myocardial infarction, stroke, transient ischemic attack, and even arrhythmia and heart failure. Endothelial dysfunction is a well-established fundamental cause of cardiovascular diseases and also a predictor of worse clinical outcomes. Accumulating evidence indicates that aldosterone plays an important role in the initiation and progression of endothelial dysfunction. Several mechanisms have been shown to contribute to aldosterone-induced endothelial dysfunction, including aldosterone-mediated vascular tone dysfunction, aldosterone- and endothelium-mediated vascular inflammation, aldosterone-related atherosclerosis, and vascular remodeling. These mechanisms are activated by aldosterone through genomic and nongenomic pathways in mineralocorticoid receptor-dependent and independent manners. In addition, other cells have also been shown to participate in these mechanisms. The complex interactions among endothelium, inflammatory cells, vascular smooth muscle cells and fibroblasts are crucial for aldosterone-mediated endothelial dysregulation. In this review, we discuss the association between aldosterone and endothelial function and the complex mechanisms from a molecular aspect. Furthermore, we also review current clinical research of endothelial dysfunction in patients with PA.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms20205214
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Aldosterone Excess Induced Mitochondria Decrease and Dysfunction via Mineralocorticoid Receptor and Oxidative Stress In Vitro and In Vivo
    MDPI AG ; 2021
    In:  Biomedicines Vol. 9, No. 8 ( 2021-08-02), p. 946-
    Details
    In: Biomedicines, MDPI AG, Vol. 9, No. 8 ( 2021-08-02), p. 946-
    Abstract: Aldosterone excess plays a major role in the progression of cardiac dysfunction and remodeling in clinical diseases such as primary aldosteronism and heart failure. However, the effect of aldosterone excess on cardiac mitochondria is unclear. In this study, we investigated the effect of aldosterone excess on cardiac mitochondrial dysfunction and its mechanisms in vitro and in vivo. We used H9c2 cardiomyocytes to investigate the effect and mechanism of aldosterone excess on cardiac mitochondria, and further investigated them in an aldosterone-infused ICR mice model. The results of the cell study showed that aldosterone excess decreased mitochondrial DNA, COX IV and SOD2 protein expressions, and mitochondria ATP production. These effects were abolished or attenuated by treatment with a mineralocorticoid receptor (MR) antagonist and antioxidant. With regard to the signal transduction pathway, aldosterone suppressed cardiac mitochondria through an MR/MAPK/p38/reactive oxygen species pathway. In the mouse model, aldosterone infusion decreased the amount of cardiac mitochondrial DNA and COX IV protein, and the effects were also attenuated by treatment with an MR antagonist and antioxidant. In conclusion, aldosterone excess induced a decrease in mitochondria and mitochondrial dysfunction via MRs and oxidative stress in vitro and in vivo.
    Type of Medium: Online Resource
    ISSN: 2227-9059
    URL: Article
    DOI: 10.3390/biomedicines9080946
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2720867-9
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  • 7
    Online Resource
    Online Resource
    Correction: Hsu et al. Development of Folic Acid-Conjugated and Methylene Blue-Adsorbed Au@TNA Nanoparticles for Enhanced Photodynamic Therapy of Bladder Cancer Cells. Nanomaterials 2020, 10, 1351
    MDPI AG ; 2023
    In:  Nanomaterials Vol. 13, No. 15 ( 2023-08-02), p. 2233-
    Details
    In: Nanomaterials, MDPI AG, Vol. 13, No. 15 ( 2023-08-02), p. 2233-
    Abstract: Within the publication of this article in Nanomaterials 2020, 10, 1351 [...]
    Type of Medium: Online Resource
    ISSN: 2079-4991
    URL: Article
    DOI: 10.3390/nano13152233
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2662255-5
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  • 8
    Online Resource
    Online Resource
    Development of Folic Acid-Conjugated and Methylene Blue-Adsorbed Au@TNA Nanoparticles for Enhanced Photodynamic Therapy of Bladder Cancer Cells
    MDPI AG ; 2020
    In:  Nanomaterials Vol. 10, No. 7 ( 2020-07-10), p. 1351-
    Details
    In: Nanomaterials, MDPI AG, Vol. 10, No. 7 ( 2020-07-10), p. 1351-
    Abstract: Photodynamic therapy (PDT) is a promising treatment for malignancy. However, the low molecular solubility of photosensitizers (PSs) with a low accumulation at borderline malignant potential lesions results in the tardy and ineffective management of recurrent urothelial carcinoma. Herein, we used tannic acid (TNA), a green precursor, to reduce HAuCl4 in order to generate Au@TNA core-shell nanoparticles. The photosensitizer methylene blue (MB) was subsequently adsorbed onto the surface of the Au@TNA nanoparticles, leading to the incorporation of a PS within the organic shell of the Au nanoparticle nanosupport, denoted as Au@TNA@MB nanoparticles (NPs). By modifying the surface of the Au@TNA@MB NPs with the ligand folate acid (FA) using NH2-PEG-NH2 as a linker, we demonstrated that the targeted delivery strategy achieved a high accumulation of PSs in cancer cells. The cell viability of T24 cells decreased to 87.1%, 57.1%, and 26.6% upon treatment with 10 ppm[Au] Au@TNA/MB NPs after 45 min, 2 h, and 4 h of incubation, respectively. We also applied the same targeted PDT treatment to normal urothelial SV-HUC-1 cells and observed minor phototoxicity, indicating that this safe photomedicine shows promise for applications aiming to achieve the local depletion of cancer sites without side effects.
    Type of Medium: Online Resource
    ISSN: 2079-4991
    URL: Article
    DOI: 10.3390/nano10071351
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2662255-5
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  • 9
    Online Resource
    Online Resource
    Geometrical Calibration of a 2.5D Periapical Radiography System
    MDPI AG ; 2020
    In:  Applied Sciences Vol. 10, No. 3 ( 2020-01-30), p. 906-
    Details
    In: Applied Sciences, MDPI AG, Vol. 10, No. 3 ( 2020-01-30), p. 906-
    Abstract: The objective of this study was to develop a geometrical calibration method applicable to the 2.5D prototype Periapical Radiography System and estimate component position errors. A two-steel-ball phantom with a precisely known position was placed in front of a digital X-ray sensor for two-stage calibration. In the first stage, the following three parameters were estimated: (1) r, the distance between the focal spot and the rotation axis of the X-ray tube; (2) ψ, the included angle between the straight line formed by the X-ray tube’s focal spot and rotation axis and the straight line of the orthogonal sensor; and (3) L4, the distance between the rotation axis and the plane where the two steel balls were positioned. In the second stage, the steel balls’ positions were determined to calculate the positions of the X-ray tube on the x, y, and z axes. Computer simulation was used to verify the accuracy of the calibration method. The results indicate that for the calibration approach proposed in this study, the differences between the estimated errors and setting errors were smaller than 0.15% in the first and second stages, which is highly accurate, verifying its applicability to accurate calibration of the 2.5D Periapical Radiography System.
    Type of Medium: Online Resource
    ISSN: 2076-3417
    URL: Article
    DOI: 10.3390/app10030906
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2704225-X
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  • 10
    Online Resource
    Online Resource
    Recombinant Aflatoxin-Degrading F420H2-Dependent Reductase from Mycobacterium smegmatis Protects Mammalian Cells from Aflatoxin Toxicity
    MDPI AG ; 2019
    In:  Toxins Vol. 11, No. 5 ( 2019-05-08), p. 259-
    Details
    In: Toxins, MDPI AG, Vol. 11, No. 5 ( 2019-05-08), p. 259-
    Abstract: Aflatoxins are carcinogenic secondary metabolites of fungi that contaminate many staple crops and foods. Aflatoxin contamination is a worldwide problem, especially in developing countries, posing health hazards, e.g., causing aflatoxicosis and hepatocellular carcinoma, and even death. Biological solutions for aflatoxin detoxification are environmentally friendly and a cheaper alternative than chemical methods. The aims of the current study were to investigate: (1) the ability of MSMEG_5998, an aflatoxin-degrading F420H2-dependent reductase from Mycobacterium smegmatis, to degrade aflatoxin B1 (AFB1) and reduce AFB1-caused damage in HepG2 cell culture model; and (2) whether a thioredoxin (Trx) linkage of MSMEG_5998 enhanced the enzyme activity. We show that Trx-linked MSMEG_5998 degraded 63% AFB1 and native MSMEG_5998 degraded 31% after 4 h at 22 °C, indicating that the Trx-linked enzyme had a better AFB1-degrading ability. In a HepG2 cell culture model, Trx-linked MSMEG_5998 reduced DNA damage and p53-mediated apoptosis caused by AFB1 to a greater extent than the native enzyme. These findings suggest that Trx-linked MSMEG_5998 could potentially be developed to protect the liver from AFB1 damage, or as a candidate protein to reduce AFB1-related toxicity in animals.
    Type of Medium: Online Resource
    ISSN: 2072-6651
    URL: Article
    DOI: 10.3390/toxins11050259
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2518395-3
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