Correlation between blood inflammatory indices and carotid intima-media thickness in the middle-aged and elderly adults.

OBJECTIVES: This study aimed to investigate the correlations between carotid intima-media thickness (IMT) and systemic immune inflammation index (SII), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte (NLR) ratio. MATERIALS AND METHODS: This was a cross-sectional study enrolling a total of 582 middle-aged and elderly patients. The correlations between SII, PLR, and NLR with IMT were assessed using logistic regression models, which were subsequently incorporated into the underlying models with traditional risk factors and their predictive values for IMT. RESULTS: NLR exhibited a significant correlation with IMT in the simple regression analysis (ß = 0.01, 95 %CI= 0.00-0.02, p < 0.05). After controlling for potential confounding variables in the multivariate analysis, the association between NLR and both Maximum IMT [ß = 0.04, 95 %CI = 0.02-0.07, p = 0.0006] and Mean IMT [ß = 0.05, 95 %CI = 0.02-0.07, p = 0.0001] remained statistically significant. Additionally, PLR was found to be a significant independent predictor of Maximum IMT [ß = 0.04, 95 % CI =0.00-0.07, p = 0.0242] and Mean IMT [ß = 0.04, 95 % CI = 0.01-0.07, p = 0.0061]. Similarly, SII was identified as an independent predictor of Maximum IMT [ß = 1.87, 95 % CI =1.24, p = 0.0003]. The study found a significant positive correlation between Maximum IMT and the levels NLR, PLR, and SII. Specifically, in the Maximum IMT group, higher quartiles of NLR, PLR, and SII were associated with increased odds ratios (OR) for elevated IMT levels, with statistically significant results for NLR (Q4vsQ1: OR 3.87, 95 % CI 1.81-8.29), PLR (Q4vsQ1: OR 2.84, 95 % CI 1.36-5.95), and SII (Q4vsQ1: OR 2.64, 95 % CI 1.30-5.37). Finally, the inclusion of NLR, PLR, and NLR+PLR+SII in the initial model with traditional risk factors resulted in a marginal improvement in the predictive ability for Maximum IMT, as evidenced by the net reclassification index (p < 0.05). CONCLUSIONS: This study discovered a positive correlation between SII, PLR, NLR, and IMT, which are likely to emerge as new predictors for IMT thickening. These findings lay a theoretical reference for future predictive research and pathophysiological research on carotid intima-media thickening.

Differential Expression and Correlation Analysis of Global Transcriptome for Hemorrhagic Transformation After Acute Ischemic Stroke.

In order to explore the epigenetic characteristics of hemorrhagic transformation (HT) after acute ischemic stroke, we used transcriptome sequencing technology to analyze the global transcriptome expression profile of patients with and without HT after acute ischemic stroke and to study the differential expression of messenger RNA (mRNA), long noncoding RNA (lncRNA), circular RNA (circRNA) and mircoRNA (miRNA) between the two groups. To further explore the role of differentially expressed genes in HT, we annotated the function of differentially expressed genes by using gene ontology (GO) and pathway analysis on the results and showed that there were 1,051 differential expressions of lncRNAs, 2,575 differential expressions of mRNAs, 447 differential expressions of circRNAs and 47 miRNAs in patients with HT compared with non-HT patients. Pathway analysis showed that ubiquitin-mediated proteolysis, MAPK signal pathway, axon guidance, HIF-1 signal pathway, NOD-like receptor signal pathway, beta-alanine metabolism, Wnt signal pathway, sphingolipid signal pathway, neuroactive ligand-receptor interaction, and intestinal immune network used in IgA production play an important role in HT. Terms such as iron homeostasis, defense response, immune system process, DNA conformational change, production of transforming growth factor beta-2, and oxidoreductase activity were enriched in the gene list, suggesting a potential correlation with HT. A total of 261 lncRNA-miRNA relationship pairs and 21 circRNA-miRNA relationship pairs were obtained; additionally, 5 circRNAs and 13 lncRNAs were screened, which can be used as competing endogenous RNA (ceRNA) to compete with miRNA in the co-expression network. Co-expression network analysis shows that these differentially expressed circRNA and lncRNA may play a vital role in HT and provide valuable information for new biomarkers or therapeutic targets.

MALAT1 Protected the Angiogenesis Function of Human Brain Microvascular Endothelial Cells (HBMECs) Under Oxygen Glucose Deprivation/re-oxygenation (OGD/R) Challenge by Interacting with miR-205-5p/VEGFA Pathway.

Long non-coding RNA MALAT1 was previously revealed to express abnormally in animal and cellular models of stroke, suggesting its indispensable role in stroke. The aims of the present study were to further investigate the functions of MALAT1 and to elucidate the underlying molecular mechanisms. Oxygen glucose deprivation/re-oxygenation (OGD/R) challenge was used in human brain microvascular endothelial cells (HBMECs) to mimic stroke injury in vitro. MALAT1 and miR-205-5p expression levels were evaluated by qRT-PCR. A tube formation assay was employed to verify the angiogenesis of HBMECs. Cell proliferation and apoptosis were evaluated using the ErdU assay and flow cytometry analysis, respectively. The interaction between miR-205-5p and MALAT1 was verified by dual-luciferase reporter assay. MALAT1 and miR-205-5p were both significantly upregulated in the serum of CIS patients and HBMECs under OGD/R, and the tube formation of HBMECs was damaged after OGD/R treatment. Silencing miR-205-5p remarkably promoted HBMEC proliferation and angiogenesis to resist OGD/R injury. Knockdown of MALAT1 markedly inhibited HBMEC proliferation and angiogenesis, and meanwhile promoted apoptosis induced by OGD/R treatment. Most importantly, MALAT1 acted as a competing endogenous RNA (ceRNA) of miR-205-5p via direct bonding with each other in HBMECs under OGD/R damage, indirectly upregulating the downstream targeted gene VEGFA. MALAT1 protected the angiogenesis function of HBMECs under OGD/R conditions by interacting with miR-205-5p/VEGFA pathway.

Effect of Interventional Therapy on IL-1ß, IL-6, and Neutrophil-Lymphocyte Ratio (NLR) Levels and Outcomes in Patients with Ischemic Cerebrovascular Disease.

BACKGROUND This study investigated the clinical effect of interventional therapy in ischemic cerebrovascular disease (ICD). MATERIAL AND METHODS A retrospective analysis was performed on 260 ICD patients who were divided into a control group (122 patients, conventional drug treatment) and an observation group (138 patients, interventional therapy plus conventional drug treatment). Enzyme-linked immunosorbent assay was used to examine the expression of IL-1ß, IL-6, and NLR. Furthermore, neurological deficit scores and Barthel index scores as well as the correlation of IL-1ß, IL-6 and NLR were examined in these 2 groups. RESULTS The expression of IL-1ß, IL-6, and NLR significantly decreased in both groups after 1 week or 4 weeks of treatment compared with before treatment (P<0.05). Significant differences in neurological impairment scores were detected between these 2 groups after 4 weeks of treatment (P<0.05), and the control group showed higher neurological deficit scores than did the observation group (P<0.05). Barthel index scores were significantly higher after treatment than before treatment in the control and observation group (P<0.05), and the control group had lower Barthel index scores than did the observation group (P<0.05). Pearson correlation analysis showed that IL-1ß, IL-6, and NLR expression were positively correlated in ICD patients (P<0.05). CONCLUSIONS Interventional surgery combined with conventional drug therapy can reduce serum IL-1ß and IL-6 levels, decrease neurological impairment, and improve the quality of life of patients. The combined treatment group showed better outcomes than did the group that received the drug alone; therefore, combined therapy is suitable for promoting better clinical outcomes.

Insulinoma Presenting as a Complex Partial Seizure: Still a Possible Misleading Factor.

Delayed diagnosis of insulinoma remains an intractable clinical challenge because the symptoms are in most cases misattributed to other disorders. In this study, a 64-year-old man presented with intermittent seizure episodes after being misdiagnosed with epilepsy and receiving anti-epileptic drugs for 4 years. During this period, the patient continued to suffer from repeated seizures. A starvation test, pancreatic enhancement CT, MRI scan, and pathological examination clinically diagnosed insulinoma, and the symptoms improved following surgical removal of the tumor. The appearance of unusual manifestations and insulinoma imaging makes it difficult to accurately diagnose the condition. This case emphasizes the need for careful reassessment of all atypical and refractory seizures for neurologists.

HDAC4 in ischemic stroke: mechanisms and therapeutic potential.

Stroke is one of the leading causes of death and disability worldwide, and the majority of the cases are ischemic stroke. However, it still lacks effective treatment except for thrombolytic therapy in an extremely narrow time window. Increased evidence suggests that histone deacetylase 4 (HDAC4) was dysregulated in ischemic stroke, which plays a key role in the pathogenesis of ischemic stroke and post-stroke recovery by affecting neuronal death, angiogenesis, and neurogenesis. Therefore, we aim to review the dysregulation of HDAC4 in ischemic stroke and the role of dysregulated HDAC4 in the pathogenesis of ischemic stroke. Furthermore, the therapeutic potential of modulating HDAC4 in ischemic stroke is discussed.

l-Homocarnosine, l-carnosine, and anserine attenuate brain oxidative damage in a pentylenetetrazole-induced epilepsy model of ovariectomized rats.

In this study, we investigated the protective effect of l-homocarnosine, l-carnosine, and anserine (HCA) on seizure-induced brain injuries. We evaluated the protective effect of HCA on brain oxidative damage in a pentylenetetrazole (PTZ)-induced epilepsy model using ovariectomized (OVX) rats. The experimental groups were as follows: group I, sham; group II, sham + PTZ; group III, sham + HCA + PTZ; group IV, OVX; group V, OVZ + PTZ; and group VI, OVX + HCA + PTZ. We determined the levels of lipid peroxidation, glutathione peroxidase (Gpx), reduced glutathione (GSH), catalase, superoxide dismutase (SOD), and thiol in brain hippocampal and cortical tissue. The biochemical markers were significantly altered in the brain tissue of OVX rats. HCA supplementation significantly reduced lipid peroxidation and increased GSH, Gpx, SOD, catalase, and thiol levels in PTZ-treated OVX rats. Rats with an ovariectomy showed a significant protective effect against PTZ through elevation of the latency of generalized tonic-clonic seizures (GTCS). HCA substantially increased minimal clonic seizure and GTCS latency in the OVX-PTZ and sham-PTZ groups. In summary, our experimental data indicate that combined supplementation of HCA substantially increased anticonvulsant activity. Moreover, combined HCA supplementation reduced oxidative damage by decreasing lipid peroxidation and increasing antioxidant levels in the brain of a PTZ-induced seizure rodent model.

Protective effects of VEGF treatment on focal cerebral ischemia in rats.

The aim of this study was to determine the effects of VEGF treatment on focal cerebral ischemia in rats. Rats were administered PBS or VEGF at concentrations of 10, 20 or 30 µg/ml. The effects of VEGF on the rat infarct volume and neurological deficits were investigated. Transmission electron microscopy was used to observe the ultrastructure of the cerebral cortex. Treatments with VEGF reduced the infarct volume and improved neurological functions. VEGF increased microvessel generation and also inhibited apoptosis in the cerebral cortex and basal ganglia. For the rats in the 30 µg/ml VEGF group, an even higher number of proliferative endothelial cells were observed by electron microscopy. In conclusion, VEGF treatment has protective effects on focal cerebral ischemia in rats.