Analysis of the Relationship Between the Changes of Serum SAA, LP-PLA2, sCD40L and Carotid Atherosclerosis Plaque in Patients with Acute Cerebral Infarction.

Objective: To explore the relationship between Serum amyloid protein A(SAA), lipoprotein-associated Phospholipase A2 (Lp-PLA2) and soluble CD40 ligand (sCD40L) in detecting the stability of carotid Atherosclerosis plaque. Methods: We examined 90 patients admitted to our hospital with acute cerebral infarction from July 2020 to December 2022. Carotid artery ultrasounds were performed for all of them. These patients were then divided into two groups: the stable plaque group (45 cases) and the unstable plaque group (45 cases), based on the ultrasound results. Additionally, we included a control group of 30 healthy individuals from our hospital. We collected fasting blood samples from the patients upon admission and used enzyme-linked immunosorbent assays to measure the mass concentrations of sCD40L, Lp-PLA2, and SAA in their serum. The results of these biomarkers were compared and analyzed to assess potential associations with plaque stability in patients with cerebral infarction. Results: Comparison of general clinical data and laboratory data: except for High-density lipoprotein, there was a statistical difference between the control group and the cerebral infarction group (P < .05), there was no statistical difference in gender, smoking history, drinking history and age (P > .05). Compared with the control group, the mass concentrations of sCD40L, Lp-PLA2, and SAA in patients with stable and unstable plaques increased significantly (P < .05); Compared with the stable plaque group, the mass concentrations of sCD40L, Lp-PLA2, and SAA in unstable plaque patients increased with statistical significance (P < .05). Correlation analysis shows that the mass concentrations of sCD40L, Lp-PLA2, and SAA are positively correlated with the stability of carotid artery plaques. SCD40L, Lp-PLA2 and SAA have certain diagnostic significance in the subject's working characteristic curve (Receiver operating characteristic) as a marker molecule for the diagnosis of unstable plaque. sCD40L (AUC=0.883) has more diagnostic value than SAA (AUC=0.756) and Lp-PLA2 (AUC=0.826). A binary logistic regression analysis was conducted using the stability of carotid artery plaques as the dependent variable and sCD40L, Lp-PLA2, and SAA as independent variables. The results showed that elevated serum sCD40L, Lp-PLA2, and SAA were independent risk factors for unstable carotid artery plaques (P < .05). Conclusion: The concentrations of sCD40L, Lp-PLA2 and SAA are closely related to the formation and type of carotid Atherosclerosis plaque in patients with acute cerebral infarction. This has potentially important clinical implications for the management and prevention of cardiovascular disease.

CircCDC45 promotes the malignant progression of glioblastoma by modulating the miR-485-5p/CSF-1 axis.

BACKGROUND: Glioblastoma (GBM) is characterized by progressive growth and metastasis. Numerous studies claim that the deregulation of circular RNAs (circRNAs) is associated with cancer progression. However, the role of circRNAs in GBM is largely limited. The purpose of this study was to investigate the functions of circCDC45 in GBM and provide a feasible functional mechanism to support its role. METHODS: The expression of circCDC45, miR-485-5p and colony-stimulating factor 1 (CSF-1) mRNA was examined using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using cell counting kit - 8 (CCK-8) assay and colony formation assay. Cell migration and cell invasion were monitored using transwell assay. The protein levels of proliferation-related markers and CSF-1 were determined using western blot. The target relationship was predicted using bioinformatics tools and validated using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Animal models were constructed to verify the role of circCDC45 in vivo. RESULTS: The expression of circCDC45 and CSF-1 was elevated in GBM tissues and cells, while the expression of miR-485-5p was declined. Downregulation of circCDC45 or CSF-1 blocked GBM cell proliferation, invasion and migration as well as tumor growth in vivo. In mechanism, circCDC45 positively regulated the expression of CSF-1 by targeting miR-485-5p. Inhibition of miR-485-5p reversed the biological effects caused by circCDC45 downregulation in GBM cells. CONCLUSION: CircCDC45 promoted the progression of GBM by mediating the miR-485-5p/CSF-1 axis, and circCDC45 might be a promising plasmatic biomarker for GBM diagnosis and treatment.

Predictive Value of Insulin Resistance as Determined by Homeostasis Model Assessment in Acute Ischemic Stroke Patients: A Systematic Review and Meta-Analysis.

Studies on association between homeostasis model assessment of insulin resistance (HOMA-IR) and adverse outcomes have yielded conflicting results in patients with acute ischemic stroke (AIS). This meta-analysis aimed to assess the predictive value of HOMA-IR in AIS patients. Two authors comprehensively searched PubMed and Embase databases until February 28, 2021. All observational studies investigating the association between HOMA-IR and adverse outcomes in AIS patients were included. Outcome measures were poor functional outcome (Modified Rankin Scale≥3), all-cause mortality, stroke recurrence, and neurologic worsening. Seven studies (eight articles) involving 8330 AIS patients were identified. For the highest versus lowest HOMA-IR, the pooled risk ratio (RR) of poor functional outcome was 2.55 (95% CI 1.76-3.70) after adjustment of conventional confounding factors. In addition, elevated HOMA-IR was associated with higher risk of neurologic worsening (RR 1.93; 95% CI 1.15-3.26). However, there were conflicting findings on the association of HOMA-IR with stroke recurrence and all-cause mortality. This meta-analysis confirms that HOMA-IR is significantly associated with an increased risk of poor functional outcome in patients with AIS. However, interpretation of the results of mortality, stroke recurrence, and neurologic worsening should be done with caution due to small number of studies available.

Cerebrospinal fluid exosomal miR-152-3p predicts the occurrence of subarachnoid haemorrhage and regulates vascular smooth muscle cell dysfunction.

INTRODUCTION: Ruptured intracranial aneurysm (RA) can lead to subarachnoid haemorrhage (SAH). This study was to explore the predictive value of cerebrospinal fluid (CSF) derived exosome miR-152-3p and its regulatory role in the human vascular smooth muscle cells (HVSMCs). MATERIAL AND METHODS: Real-time quantitative polymerase reaction was carried out to detect CSF exosome miR-152-3p in 66 patients with unruptured intracranial aneurysms (UA), 69 patients with RA, and 68 patients with hydrocephalus. Clinical predictive value of SAH occurrence was assessed using receiver operating characteristic curve (ROC) and logistics regression analysis. Cell Counting Kit-8 and Transwell were employed to detect the proliferation and migration of HVSMCs. The binding relationship between miR-152-3p and PTEN was confirmed by the dual-luciferase reporter assay. RESULTS: Compared with hydrocephalus, exosome miR-152-3p was lower in patients with intracranial aneurysms, and among them, RA was lower than in patients with UA (p < 0.001). ROC confirmed that exosome miR-152-3p not only distinguishes patients with UA from patients with hydrocephalus but also predicts SAH in patients with intracranial aneurysms. Logistic regression analysis showed that miR-152-3p (OR = 0.039, 95% CI = 0.015-0.106, p < 0.001) and aneurysm size (OR = 2.701, 95% CI = 1.045-6.890, p = 0.040) were independent predictors of progression for UA to RA. Increased miR-152-3p inhibited the proliferation and migration of HVSMCs. PTEN was the direct target gene of miR-152-3p, which was elevated in CSF-derived exosomes and negatively correlated with miR-152-3p levels. CONCLUSIONS: Our study confirmed that the CSF-derived exosome miR-152-3p was a feasible predictor of SAH and was involved in the dysfunction of HVSMCs.

Lycopene attenuates early brain injury and inflammation following subarachnoid hemorrhage in rats.

Early brain injury (EBI), following subarachnoid hemorrhage (SAH), includes blood-brain barrier (BBB) disruption and consequent edema formation. This study aims to evaluate the effect of lycopene on early brain injury and inflammation in SAH. Neurological deficits, brain water content and Evans blue dye extravasation were evaluated after the treatment with lycopene. Besides neuronal apoptosis,some inflammatory cytokines were also detected. The results suggested that administration of lycopene following SAH significantly ameliorated EBI, including brain edema, blood-brain barrier (BBB) impairment, cortical apoptosis, and neurological deficits. In addition, it also ameliorated inflammation triggered by SAH. In conclusion, post-SAH lycopene administration may attenuate EBI in SAH, possibly through ameliorating neuronal apoptosis, maintaining BBB integrity and attenuating inflammation.

[Treatment of thoracolumbar burst fracture with subtotal vertebrectomy, decompression and strut grafting through posterolateral approach].

OBJECTIVE: To explore the clinical effect of subtotal vertebrectomy, decompression and strut grafting in treating thoracolumbar burst fractures through posterolateral approach via posterior midline incision. METHODS: From May 2005 to July 2008, 14 patients with thoracolumbar burst fractures were treated with subtotal vertebrectomy, decompression and strut grafting through posterolateral approach via posterior midline incision. There were 9 males and 5 females, ranging in age from 24 to 68 years, with an average of 42.3 years. All patients were single segment fractures, of them, T11 was in 1 case, T12 in 5, L1 in 5 and L2 in 3. According to AO classification in spinal fracture, type A3 was in 5 cases, B1 in 3, B2 in 3, C1 in 2, C2 in 1. According to the ASIA classification in neurological function, grade A was in 3 cases, B in 3, C in 5, D in 2, E in 1. The height of anterior border vertebral body, volume of spinal canal and neurological function were analyzed by X-ray films, CT scanning and ASIA classification preoperative, postoperative and at final follow-up. RESULTS: Operative time was from 3.5 to 5.5 hours with the mean of 4.0 hours; bleeding during operation was from 800 to 2 600 ml with the mean of 1 300 ml. Two cases with nerve root injury recovered without special handling after 3-6 months; 1 case with leakage of cerebrospinal fluid restored through lumbar cerebrospinal fluid drainage; 1 case with pleura tear healed through closed thoracic drainage. No iatrogenic vascular injury or infection was found. The follow-up time was from 8 to 36 months with the mean of 16.5 months. All patients had neurofunctional recovery at different degree, except that 3 patients in grade A. The height of anterior border vetebral body restored from (42.25 +/- 11.87)% preoperatively to (94.38 +/- 3.08)% postoperatively, and (92.87 +/- 3.32)% at final follow-up (P<0.05); volume of spinal canal (the actual volume of spinal canal/normal volume of spine canal) increased from (45.63 +/- 6.88)% preoperatively to (95.26 +/- 3.31)% postoperatively, and (96.13 +/- 2.56)% at final follow-up (P<0.05). Cobb angle were corrected from (25.64 +/- 4.40) degrees preoperatively to (5.80 +/- 1.14) degrees postoperatively; Cobb angle lost from 0 degrees to 6 degrees at final follow-up with (8.10 +/- 2.65) degrees. All patients obtained complete bony fusion without pseudarthrosis formation at final follow-up. CONCLUSION: Subtotal vertebrectomy decompression and strut grafting through posterolateral approach via posterior midline incision is an effective and safe method in treating thoracolumbar burst fracture, which can restored height of intervertebral body, volume of spinal canal and physiological flexion of spinal column, and retain spinal permanent stability.