Role of long non-coding RNA TCONS_02443383 in regulating cell adhesion and peroxisome proliferator-activated receptor (PPAR) signaling genes in atherosclerosis: A New Zealand white rabbit model study.

OBJECTIVE: In this study, we performed RNA sequencing (RNA-seq) on the abdominal aorta tissue of New Zealand rabbits and investigated the potential association of lncRNA TCONS_02443383 with the development of AS through bioinformatics analysis of the sequencing data. The obtained results were further validated using quantitative real-time polymerase chain reaction (qRT-PCR). METHOD: We induced an AS model in New Zealand rabbits by causing balloon injury to the abdominal aorta vascular wall and administering a high-fat diet. We then upregulated the expression level of the lncRNA TCONS_02443383 by injecting lentiviral plasmids through the ear vein. RNA sequencing (RNA-seq) was performed on the abdominal aorta tissues. We conducted Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway and Gene Ontology (GO) analyses. RESULT: The overexpression of the lncRNA TCONS_02443383 led to an upregulation of peroxisome proliferator-activated receptor (PPAR) signaling pathways as well as genes related to cell adhesion. CONCLUSION: The overexpression of the lncRNA TCONS_02443383 can inhibit the occurrence and development of AS by upregulating peroxisome proliferator-activated receptor (PPAR) signaling pathways and genes related to cell adhesion.

A Study of Spontaneous Brain Activity on Resting-State Functional Magnetic Resonance Imaging in Adults with MRI-Negative Temporal Lobe Epilepsy.

Purpose: Patients with magnetic resonance imaging (MRI)-negative temporal lobe epilepsy (TLE-N) represent an important subgroup of temporal lobe epilepsy (TLE). Here, we aimed to combine three voxel-based local brain area analysis methods of resting-state functional MRI (rs-fMRI), to examine the TLE-N patients' resting brain function based on neural synchronization and intensity of local brain areas. Methods: The study included 47 patients with TLE, including 28 cases of drug-controlled TLE (cTLE-N) and 19 cases of drug-resistant TLE-N (rTLE-N), as well as 30 participants in the healthy control (HC) group. To comprehensively assess the altered brain function associated with TLE-N patients, we analyzed three data-driven rs-fMRI algorithms for amplitude of low-frequency fluctuations (ALFF), fractional ALFF (fALFF) and regional homogeneity (ReHo). Results: Compared to the HC group, the distribution of abnormal functional brain areas in cTLE-N patients was dominated by occipital lobe activation, as measured by increased fALFF values in the superior occipital gyrus (SOG) and increased ReHo values in the lingual gyrus (Lin), fusiform gyrus, and middle occipital gyrus. Patients with rTLE-N exhibited a diffuse distribution of abnormal functional brain areas, showing increased fALFF values in the SOG, Lin, superior temporal gyrus, and postcentral gyrus, and decreased fALFF values in the inferior frontal gyrus orbital, parahippocampal gyrus, and superior frontal gyrus orbital. The ReHo values were reduced in the orbital region of the middle frontal gyrus, the precuneus, and the parietal inferior angular gyrus; while ReHo values were elevated values in several frontal, temporal, occipital, and subcortical brain areas. Conclusion: Patients with rTLE-N have local brain activity changes in the prefrontal limbic system and default model network dysfunction, while cTLE-N patients have local brain activity changes in the visual functional areas. Different epilepsy networks exist between cTLE-N and rTLE-N.

Predictive power of high-resolution vessel wall magnetic resonance imaging in ischemic stroke.

BACKGROUND AND OBJECTIVE: Intracranial atherosclerotic disease (ICAD) is a key contributor to ischemic stroke and has a high recurrence rate. This study aimed to investigate the function of high-resolution vessel wall MRI (HR-VW-MRI) and evaluate plaque characteristics in patients with ICAD. METHODS: A consecutive series of patients with ICAD who underwent HR-VW-MRI were enrolled, and imaging measurements were acquired. Baseline clinical characteristics were identified. Telephone follow-up was conducted every three months. The endpoint events were the first onset or recurrence of ischemic stroke and new clinical vascular events. Patients were divided into groups with or without events according to whether the endpoint event occurred. RESULTS: A total of 70 patients (mean age = 57.6 years old) were enrolled. The median follow-up duration was 182 days. During the follow-up, 10 patients developed ischemic stroke, experienced endpoint events, and were found with 44 plaques in the artery area. A total of 169 plaques were further found in 70 patients. There were significant differences in EI, HST1, surface features, and WA reference between the two groups (P < 0.05). Logistic analysis showed that grade 2 enhancements, stenosis degree ≥ 50%, HST1, and surface features were independent prognostic factors of the onset of stroke, caused by ICAD. CONCLUSION: This prospective study demonstrates that HR-VW-MRI can identify atherosclerotic plaques in the cerebral artery and high-risk plaques, which may contribute to the prevention of ICAD and guide clinical treatment.

Novel Neuroimaging Biomarker for Sleep Quality in Insomnia Disorder: A Hypothalamus Resting State Study.

Despite striking progress in the understanding of the neurobiology of insomnia disorder (ID), about 40% of ID patients do not reach sustained remission with the primary treatments. It is necessary to reveal novel neuroimaging biomarkers for sleep quality in ID. The hypothalamus has a central role in sleep-wake regulation by communicating with different brain regions. However, the functional implications of hypothalamus circuitry with other brain areas remains largely unknown in ID. It may be speculated that dysfunctional circuitry in the hypothalamus is involved in the pathogenesis of ID. Thus, we investigated the different network organizations of the bilateral hypothalamus during the resting-state between 26 ID patients and 28 healthy controls (HC). Correlation analysis has been carried out to link the neuroimaging findings and Pittsburgh sleep quality index (PSQI) scores. Group comparisons reveal that the resting-state functional connectivity (RSFC) between the left hypothalamic region and a few other brain regions, including the medial prefrontal cortex (mPFC) and pallidum, are significantly higher in ID compared with HC. The right inferior temporal cortex showed reduced RSFC with the left hypothalamus. No significantly different RSFC between ID and HC was detected for the right hypothalamus. Positive correlations with PSQI scores were observed for RSFC strength between the left hypothalamus and bilateral mPFC (left: r = 0.2985, p = 0.0393; right: r = 0.3723, p = 0.0056). Similarly, the RSFC strength between the right hypothalamus and bilateral mPFC (left: r = 0.3980, p = 0.0029; right: r = 0.2972, p = 0.0291) also showed significant positive correlations with PSQI scores. In conclusion, we reveal a novel neuroimaging biomarker for sleep quality, i.e., the RSFC strength of the hypothalamus-mPFC pathway. Consistent with the hyperarousal model of ID, our results shed new insights into the implications of the hyper-connection within hypothalamus circuits in the pathology of the ID.

Three-dimensional intra- and extracranial arterial vessel wall joint imaging in patients with cerebrovascular disease.

PURPOSE: To evaluate the clinical performance of a newly developed three-dimensional (3D) intra- and extracranial arterial vessel wall joint imaging technique at 3T using T1-weighted 3D variable-flip-angle turbo spin-echo sequence with improved cerebrospinal fluid suppression in patients with cerebrovascular disease. MATERIALS AND METHODS: 122 consecutive patients (mean age 45.96 ± 12.16 years) with clinically confirmed cerebrovascular symptoms were imaged using a 3D intra- and extracranial arterial vessel wall joint imaging sequence with and without contrast enhancement on a 3 T MR system. The number of plaques and culprit plaques were evaluated. The image quality score, percent stenosis, remodeling ratio, and plaque burden were measured and compared between intracranial and carotid arterial plaques, and between non-culprit and culprit plaques. RESULTS: Except for 23 patients, there were 322 plaques (111 culprit plaques) detected in 96 patients with large artery atherosclerosis. Of the plaques, 278 (96 culprit plaques) and 44 (15 culprit plaques) plaques were identified in intracranial and extracranial arteries, respectively. Image quality did not differ significantly between pre- and post-contrast vessel wall magnetic resonance images. There were also no significant differences in the percent stenosis, remodeling ratio, and plaque burden between intracranial and carotid arteries, and between non-culprit and culprit plaques. The enhancement rate of culprit plaques was significantly higher than that of non-culprit plaques. CONCLUSIONS: The described joint imaging is a promising vessel wall magnetic resonance imaging method for comprehensive diagnosis of cerebrovascular symptoms and investigation of etiology. The imaging technique is a potentially valuable means to optimize treatment.