Lithium-Modified TiO2 Surface by Anodization for Enhanced Protein Adsorption and Cell Adhesion.

Promoting osseointegration is an essential step in improving implant success rates. Lithium has gradually gained popularity for promoting alkaline phosphatase activity and osteogenic gene expression in osteoblasts. The incorporation of lithium into a titanium surface has been reported to change its surface charge, thereby enhancing its biocompatibility. In this study, we applied anodization as a novel approach to immobilizing Li on a titanium surface and evaluated the changes in its surface characteristics. The objective of this study was to determine the effect of Li treatment of titanium on typical proteins, such as albumin, laminin, and fibronectin, in terms of their adsorption level as well as on the attachment of osteoblast cells. Titanium disks were acid-etched by 66 wt % H2SO4 at 120 °C for 90 s and set as the control group. The etched samples were placed in contact with an anode, while a platinum bar served as the counter electrode. Both electrodes were mounted on a custom electrochemical cell filled with 1 M LiCl. The samples were anodized at constant voltages of 1, 3, and 9 V. Scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM) results showed no significant differences in the topography. However, the ζ potentials of the 3 V group were higher than those of the control group at a physiological pH of 7.4. Interestingly, the adsorption level of the extracellular matrix protein was mostly enhanced on the 3 V-anodized surface. The number of attached cells on the Li-anodized surfaces increased. The localization of vinculin at the tips of the stretching cytoplasmic projections was observed more frequently in the osteoblasts on the 3 V-anodized surface. Although the optimal concentration or voltage for Li application should be investigated further, this study suggests that anodization could be an effective method to immobilize lithium ions on a titanium surface and that modifying the surface charge characteristics enables a direct protein-to-material interaction with enhanced biological adhesion.

Serum histone deacetylase 4 longitudinal change for estimating major adverse cardiovascular events in acute coronary syndrome patients receiving percutaneous coronary intervention.

OBJECTIVE: Histone deacetylase 4 (HDAC4) regulates lipid accumulation, inflammation, endothelial injury, and atherosclerosis to participate in the pathogenesis of cardiovascular diseases. This study aimed to explore the value of serum HDAC4 change before and after percutaneous coronary intervention (PCI) in predicting major adverse cardiovascular events (MACE) risk in acute coronary syndrome (ACS) patients. METHODS: HDAC4 from serum was detected by enzyme-linked immunosorbent assay in 340 ACS patients at baseline, day (D)1, D3, and D7 after PCI, and from 30 healthy controls (HCs). MACE was recorded during follow-up. RESULTS: HDAC4 was decreased in ACS patients versus HCs (P < 0.001). In ACS patients, HDAC4 was negatively related to total cholesterol (P = 0.025), low-density lipoprotein cholesterol (P = 0.007), C-reactive protein (P < 0.001), cardiac troponin I (P < 0.001), and hyperlipidemia history (P = 0.015). Additionally, HDAC4 was lowest in ST-elevation myocardial infarction (STEMI) patients, followed by non-STEMI patients, and highest in unstable angina patients (P = 0.010). After PCI, HDAC4 was decreased from baseline to D1, then increased until D7 (P < 0.001). Furthermore, HDAC4 at baseline (P = 0.002), D1 (P < 0.001), D3 (P < 0.001), and D7 (P < 0.001) were all reduced in patients who experienced MACE versus those who did not. Meanwhile, high HDAC4 at baseline (P = 0.036), D1 (P = 0.010), D3 (P = 0.012), and D7 (P = 0.012) estimated decreased accumulating MACE risk by Kaplan-Meier curve. Multivariate logistic analysis revealed that HDAC4 at D1 was independently linked to lower MACE risk (odds ratio = 0.957, P = 0.039). CONCLUSION: Serum HDAC4 is decreased from baseline to D1, then elevated until D7, and its increased level correlates with lower MACE risk in ACS patients receiving PCI.

The abnormal level and prognostic potency of multiple inflammatory cytokines in PCI-treated STEMI patients.

OBJECTIVE: Inflammatory cytokines modulate atherogenesis and plaque rupture to involve in ST-segment elevation myocardial infarction (STEMI) progression. The present study determined eight inflammatory cytokine levels in 212 percutaneous coronary intervention (PCI)-treated STEMI patients, aiming to comprehensively investigate their potency in estimating major adverse cardiac event (MACE) risk. METHODS: Serum tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, IL-8, IL-10, IL-17A, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) of 212 PCI-treated STEMI patients and 30 angina pectoris patients were determined using enzyme-linked immunosorbent assay. RESULTS: TNF-α (52.5 (43.9-62.6) pg/ml versus 46.4 (39.0-59.1) pg/ml, p = 0.031), IL-8 (61.6 (49.6-81.7) pg/ml versus 46.7 (32.5-63.1) pg/ml, p = 0.001), IL-17A (57.4 (45.7-77.3) pg/ml versus 43.2 (34.2-64.6) pg/ml, p = 0.001), and VCAM-1 (593.6 (503.4-811.4) ng/ml versus 493.8 (390.3-653.7) ng/ml, p = 0.004) levels were elevated in STEMI patients compared to angina pectoris patients, while IL-1ß (p = 0.069), IL-6 (p = 0.110), IL-10 (p = 0.052), and ICAM-1 (p = 0.069) were of no difference. Moreover, both IL-17A high (vs. low) (p = 0.026) and VCAM-1 high (vs. low) (p = 0.012) were linked with increased cumulative MACE rate. The multivariable Cox's analysis exhibited that IL-17A high (vs. low) (p = 0.034) and VCAM-1 high (vs. low) (p = 0.014) were independently associated with increased cumulative MACE risk. Additionally, age, diabetes mellitus, C-reactive protein, multivessel disease, stent length, and stent type were also independent factors for cumulative MACE risk. CONCLUSION: IL-17A and VCAM-1 high level independently correlate with elevated MACE risk in STEMI patients, implying its potency in identifying patients with poor prognoses.

Spectroscopic, stability and radical-scavenging properties of a novel pigment from gardenia.

A novel pigment, named gardecin, has been isolated from gardenia fruits, together with another five known crocins. The pigment, which possessed a structure which is unique among crocins, was characterised using spectrometric techniques, particularly 1D and 2D NMR. The NMR assignments were based on data from (1)H NMR, (13)C NMR, DEPT, (1)H-(1)H COSY, NOESY, HMQC and HMBC measurements. The five known crocins were identified on the basis of MS, UV/visible and 1D NMR data. Chemical stability and antioxidant ability of gardecin in comparison with the other five crocins were studied. The stronger DPPH free radical-scavenging ability of gardecin compared, with the other crocins, was observed. Kinetic studies have shown that all crocins were unstable under various conditions, but surprisingly gardecin was fairly stable.