LncRNA FOXD3-AS1 Contributes to Glioblastoma Progression Via Sponging miR-3918 to Upregulate CCND1.

AIM: To elucidate the pro-tumorigenic role of IncRNA FOXD3-AS1 in glioblastoma. MATERIAL AND METHODS: The expression of miR-3918, FOXD3-AS1, and CCND1 was measured in glioblastoma cells and tissues using reverse transcriptase quantitative PCR (RT-qPCR). The effect of FOXD3-AS1 silencing on the proliferation of glioblastoma cells was assessed in vitro using CCK-8 and colony formation assays and in vivo using xenograft mouse models. Additionally, the expression levels of the apoptosis-related proteins, Bcl-2 and Bax, were assessed using western blotting. Bioinformatic analysis and luciferase reporter assays assisted by RNA immunoprecipitation (RIP) and RNA pull-down experiments were conducted to validate the interactions among FOXD3-AS1, CCND1, and miR-3918. RESULTS: FOXD3-AS1 and CCND1 were highly expressed in glioblastoma tissues and cells, whereas miR-3918 was poorly expressed. The expressions of FOXD3-AS1 and CCND1 were inversely associated with miR-3918 levels in glioblastoma tissues. FOXD3-AS1 silencing weakened the proliferative capacity and accelerated apoptosis of glioblastoma cells in vitro and hampered tumor growth in vivo. Mechanical investigations showed that FOXD3-AS1 knockdown increased miR-3918 expression and inhibited glioblastoma cell growth. Meanwhile, the miR-3918 inhibitor restored CCND1 expression and induced the opposite outcome. CONCLUSION: FOXD3-AS1 facilitates the CCND1-driven progression of glioblastoma by serving as a competing endogenous RNA (ceRNA) for miR-3918. This suggests that FOXD3-AS1 may be a potential therapeutic target for the management of glioblastoma development.

Analysis of the effects of stent-induced deformation on the hemodynamics of MCA aneurysms.

The use of a stent to coil an aneurysm can alter the position of the main blood vessel and affect blood flow within the sac. This study thoroughly examines the impact of stent-induced changes on the risk of MCA aneurysm rupture. The research aims to assess the effects of coiling and vessel deformation on blood flow dynamics by comparing the OSI, WSS, and blood structure of two distinct MCA aneurysms to identify high-risk areas for hemorrhage. Computational fluid dynamics is used to model blood flow. The results indicate that aneurysm deformation does not always decrease the risk of rupture, and coiling is more effective in occluding blood flow than aneurysm deformation.

Association between Serum 25-Hydroxyvitamin D and Abdominal Aortic Calcification: A Large Cross-Sectional Study.

In the American population, the relationship between the standardized serum 25-hydroxyvitamin D (25(OH)D) concentration and the risk of abdominal aortic calcification (AAC) is unclear. The purpose of our study was to investigate the relationship between serum 25(OH)D concentration and AAC risk. Participants from the National Health and Nutrition Examination Survey (NHANES) between 2013 and 2014 were analyzed cross sectionally. An analysis of the relationship between serum 25(OH)D concentration and incident AAC and severe AAC (SAAC) was based on the restricted cubic spline (RCS) and multivariable logistic regression model. In addition, generalized additive models with smooth functions were used to evaluate the relationship between serum 25(OH)D concentration and the degree of AAC. Finally, a subgroup analysis was conducted. There were a total of 3,040 individuals in our study. The serum 25(OH)D concentration was divided into quartiles (Q1: 9.37-50.5 nmol/L; Q2: 50.6-67.2 nmol/L; Q3: 67.3-85.8 nmol/L; and Q4: 85.9-318.0 nmol/L); the lowest quartile served as the reference group (Q1). After adjusting for known confounding variables, compared with the lowest quartile (Q1) of serum 25(OH)D concentration, the odds ratios with 95% confidence intervals for AAC and SAAC across the quartiles (Q2, Q3, and Q4) were (1.042 (0.812, 1.338), 0.863 (0.668, 1.115), and 1.022 (0.787, 1.327)) and (1.48 (0.87, 2.52), 1.70 (1.01, 2.92), and 2.13 (1.19, 3.86)), respectively. As shown by the RCS plot, the serum 25(OH)D concentration was associated with the risk of AAC/SAAC in a U-shaped pattern (P for nonlinearity <0.05). In addition, the degree of AAC decreased at first and then increased as the serum 25(OH)D concentration increased. In conclusion, a U-shaped relationship existed between serum 25(OH)D concentration and the risk of AAC and SAAC. Consequently, the risk of AAC and SAAC may be mitigated with regular monitoring and vitamin D supplementation.

Correlation analysis between the static and the changed neutrophil-to-lymphocyte ratio and in-hospital mortality in critical patients with acute heart failure.

OBJECTIVE: Association between neutrophil-to-lymphocyte ratio (NLR) on admission and poor prognosis in patients with acute heart failure (AHF) has been well established. However, the relationship between dynamic changes in NLR and in-hospital mortality in AHF patients has not been studied. Our purpose was to determine if an early change in NLR within the first week after AHF patients was admitted to intensive care unit (ICU) was associated with in-hospital mortality. METHODS: Data from the medical information mart for intensive care IV (the MIMIC-IV) database was analyzed. The effect of baseline NLR on in-hospital mortality in critical patients with AHF was evaluated utilizing smooth curve fitting and multivariable logistic regression analysis. Moreover, comparison of the dynamic change in NLR among survivors and non-survivors was performed using the generalized additive mixed model (GAMM). RESULTS: There were 1169 participants who took part in the present study, 986 of whom were in-hospital survivors and 183 of whom were in-hospital non-survivors. The smooth curve fitting revealed a positive relationship between baseline NLR and in-hospital mortality, and multivariable logistic regression analysis indicated that baseline NLR was an independent risk factor for in-hospital mortality (OR 1.04, 95% CI 1.02,1.07, P-value = 0.001). After adjusting for confounders, GAMM showed that the difference in NLR between survivors and non-survivors grew gradually during the first week after ICU admission, and the difference grew by an average of 0.51 per day (ß = 0.51, 95% CI 0.45-0.56, P-value <0.001). CONCLUSIONS: Baseline NLR was associated with poor prognosis in critical patients with AHF. Early rises in NLR were linked to higher in-hospital mortality, which suggests that keeping track of how NLR early changes might help identify short-term prognosis of critical patients with AHF.

MicroRNA-485-5p inhibits glioblastoma progression by suppressing E2F transcription factor 1 under cisplatin treatment.

Cisplatin (CDDP) has been widely used for glioblastoma treatment. miR-485-5p and E2F transcription factor 1 (E2F1) dysfunction has been reported in glioblastoma. Nonetheless, whether CDDP affects glioblastoma progression via the miR-485-5p-E2F1 axis requires investigation. The expression of miR-485-5p and E2F1 was investigated by quantitative real-time polymerase chain reaction or western blotting in glioblastoma tissues and cell lines. The interaction between miR-485-5p and E2F1 was confirmed using a luciferase assay. The malignancy of glioblastoma was detected using Cell Counting Kit-8, bromodeoxyuridine (BrdU), cell adhesion, flow cytometry, and transwell assays. We identified miR-485-5p downregulation and E2F1 upregulation in glioblastoma, and miR-485-5p inhibited cell growth and elevated cell apoptosis in glioblastoma cells after CDDP treatment. Moreover, miR-485-5p targeting E2F1 repressed cell growth and improved cell apoptosis in glioblastoma cells after CDDP treatment. Our study revealed that CDDP retarded glioblastoma cell development via the miR-485-5p-E2F1 axis, which may be a new direction for glioblastoma therapy.

Homer1a protects against neuronal injury via PI3K/AKT/mTOR signaling pathway.

Purpose: Homer1a is a member of the post-synaptic density protein family that plays an important role in neuronal synaptic activity and is extensively involved in neurological disorders. The aim of this study is to investigate the role of Homer1a in modulating neuronal survival using an in vitro traumatic neuronal injury model.Materials and methods: Neurons were extracted from rats and identifited. Then, the cells were treated with Homerla overexpression or interference vectors. Western blot was performed to evaluate the expression of Homerla, apoptosis-related proteins(caspase3, caspase8, caspase9, Fasl, Bax, and p53), autophagy-related proteins (LC3ll and Beclin1), and the activiation of PI3K/AKT/mTOM pathway. In addition, the cell viability and apoptosis rate were measured. Results: After transfection with overexpression or interference vectors, the mRNA and protein expression of Homer1a increased or decreased significantly, respectively. Upregulation of Homer1a significantly alleviated apoptosis and enhanced cell viability and autophagy after traumatic neuronal injury. Homer1a overexpression also significantly decreased the expression of the pro-apoptosis proteins caspase 3, caspase 8, caspase 9, Fasl, Bax, and p53 in neurons. Furthermore, neuron autophagy was increased after traumatic neuronal injury as demonstrated by the greater accumulation of autophagosomes and higher expression of LC3II and Beclin1 induced by Homer1a overexpression. In addition, Homer1a overexpression inhibited the activation of PI3K/AKT/mTOR signaling. Conclusion: These findings indicated that Homer1a potentially protects neurons from traumatic injury by regulating apoptosis and autophagy via the caspase and PI3K/AKT/mTOR signaling pathways and may be an effective intervention target in traumatic brain injury.

Endoscopic Surgery versus External Ventricular Drainage Surgery for Severe Intraventricular Hemorrhage.

The efficacy and applied value of endoscopic hematoma evacuation vs. external ventricular drainage (EVD) in the treatment of severe ventricular hemorrhage (IVH) were explored and compared. From Jan. 2015 to Dec. 2016, the clinical data of 42 cases of IVH were retrospectively analyzed, including 18 patients undergoing endoscopic hematoma evacuation (group A), and 24 patients receiving EVD (group B). The hematoma clearance rate was calculated by 3D Slicer software, and complications and outcomes were compared between the two groups. There were no significant differences in age, sex and Graeb score between groups A and B (P>0.05). The hematoma clearance rate was 70.81%±27.64% in group A and 48.72%±36.58% in group B with a statistically significant difference (P<0.05). The operative time in groups A and B was 72.45±25.26 min and 28.54±15.27 min, respectively (P<0.05). The Glasgow Coma Scale (GCS) score increased from 9.28±2.72 at baseline to 11.83±2.91 at 1 week postoperatively in group A, and from 8.25±2.62 at baseline to 10.79±4.12 at 1 week postoperatively in group B (P<0.05). The length of hospital stay was 12.67±5.97 days in group A and 17.33±8.91 days in group B with a statistically significant difference (P<0.05). The GOS scores at 6 months after surgery were 3.83±1.12 in group A, and 2.75±1.23 in group B (P<0.05). These results suggested that endoscopic hematoma evacuation has an advantage of a higher hematoma clearance rate, fewer complications and better outcomes in the treatment of severe IVH, indicating it is a safe, effective and promising approach for severe IVH.

Effect of minocycline postconditioning and ischemic postconditioning on myocardial ischemia-reperfusion injury in atherosclerosis rabbits.

This study examined the protective effect of ischemic postconditioning (IPoC) and minocycline postconditioning (MT) on myocardial ischemia-reperfusion (I/R) injury in atherosclerosis (AS) animals and the possible mechanism. Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model. AS rabbits were randomly divided into 3 groups: (1) I/R group, the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h; (2) IPoC group, the myocardial ischemia lasted for 35 min, and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles (R20s/I20s×3)], and then reperfusion was sustained for 12 h; (3) MT group, minocycline was intravenously injected 10 min before reperfusion. The blood lipids, malondialdehyde (MDA), superoxide dismutase (SOD), soluble cell adhesion molecule (sICAM), myeloperoxidase (MPO), and cardiac troponin T (cTnT) were biochemically determined. The myocardial infarction size (IS) and apoptosis index (AI) were measured by pathological examination. The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the AS models were successfully established. The myocardial IS, the plasma levels of MDA, sICAM, MPO and cTnT, and the enzymatic activity of MPO were significantly decreased, and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group (P<0.05 for all). The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group (all P<0.05). It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits, and the mechanisms involved anti-oxidation, anti-inflammation, up-regulation of bcl-2 expression and down-regulation of caspase-3 expression. Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.

[Comparison of the exposure rates of risk factors and inducing factors of acute myocardial infarction between younger and aged adults].

OBJECTIVE: To study the clinical characteristics of acute myocardial infarction (AMI) among younger adults and to explore the possible mechanisms of early myocardial infarction, combined with the newly discovered risk factors of coronary heart disease. METHODS: Data on comparative analysis to the exposure rates of the risk factors and inducing factors of non-CAD patients with two groups of AMI patients including younger adults group (< or =40 years old) and aged adults group (> or =50 years old). Coronary angiography was applied. RESULTS: There were differences noticed between the frequencies of risk factors of the two AMI groups. In younger adults group the exposure rates of smoking, hyperlipidemia, positive family history, C-reactive protein (CRP) and fibrinogen were markedly higher, while in elderly group the exposure rates of hypertension, smoking, hyperlipidemia, diabetes, CRP, fibrinogen and homocysteine (HCY) were markedly higher (P < 0.05). Although the clustering status of risk factors of the younger adult group was not higher than that of the elderly group. There were obvious inducing factors before the patients were attacked by AMI and the inducing factors inclined to cluster, which had obvious dose-reaction relationships with the occurrence of AMI in young people. CONCLUSION: Early AMI of younger adults might relate to the clustering status of inducing factors. The coexistence of several kinds of inducing factors was resulted in the occurrence of AMI of the atherosclerosis (As) and non-As patients by means of myocardial ischemia accumulation effect.