Association Between Atherogenic Index of Plasma and Risk of Incident Major Adverse Cardiovascular Events.

It is unclear whether the atherogenic index of plasma (AIP) is associated with major adverse cardiovascular events (MACEs) in the general population. A total of 361,644 participants (aged 56.19 ± 8.09 years; 44.79% male) free of a history of MACEs at baseline from the UK Biobank data were included in the analysis. The AIP was calculated using log (triglyceride/high-density lipoprotein-cholesterol). Over a mean follow-up of 12.19 ± 1.60 years, 16,683 participants developed MACEs. After adjustment for traditional risk factors, each 1 unit increase in AIP was associated with a 45.3% higher risk of incident MACEs (hazard ratio (HR), 1.453 [95% confidence interval (CI) 1.371-1.540], P < 0.001). Results were similar when individuals were categorized by the AIP quartiles (HR, 1.283 [95% CI 1.217-1.351]; comparing extreme quartiles). The subgroup analyses showed that the association between AIP and risk of incident MACEs was more obvious in female participants who are < 60 years old and free of hypertension or diabetes. Sensitivity analysis included participants without any lipid-lowering medication or excluded incident MACEs in the first 2 years of follow-up confirming the robustness of the findings. Elevated AIP is a risk factor of incident MACEs in the general population, independent of traditional risk factors.Dynamic monitoring of the AIP may help select the population at high risk of cardiovascular events and guide primary prevention.

An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.

Background: Baicalin has been shown to promote spatial learning and neural regeneration, which might increase the differentiation of neural stem cells in Alzheimer's disease (AD) rat models. We aimed to study the role of baicalin on neuronal pentraxin-1 (NPTX-1), neuronal pentraxin-2 (NPTX-2), and C-reactive protein (CRP) in AD model rats. Methods: The 30 male Sprague Dawley rats were divided into three groups: the control group, the AD model group, and the AD + baicalin group. Then, the Morris water maze was used to verify the effect of baicalin on the memory and spatial learning of rats. Immunohistochemistry and immunofluorescence were used to observe the expression of NPTX-1, NPTX-2, and CRP in brain tissue. Results: Compared with the AD model group, the AD rats treated with baicalin spent significantly less time finding escape latencies (P = 0.008) and had longer cross-platform times in the target quadrant (P = 0.015). In addition, the AD + baicalin group had significantly higher numbers of hippocampal neurons compared with the AD model group (P < 0.05). Baicalin also obviously decreased the apoptosis of neurons. Moreover, compared with the AD model group, the NPTX-1 and CRP expression in the AD + baicalin group was significantly reduced (P = 0.000) while the expression of NPTX-2 in the brain tissue of AD rats was significantly increased (P = 0.000). Conclusions: Baicalin can play a therapeutic role by downregulating NPTX-1, upregulating NPTX-2, and downregulating CPR in AD model rats.

LncRNA nuclear-enriched abundant transcript 1 aggravates cerebral ischemia/reperfusion injury through activating early growth response-1/RNA binding motif protein 25 axis.

Ischemic stroke is a major global health issue. Ischemia and subsequent reperfusion results in stroke-related brain injury. Previous studies have demonstrated that nuclear-enriched abundant transcript 1 (NEATa and early growth response 1 (EGR1) are involved in ischemia reperfusion (IR) injury). In this study, we aimed to explore the roles of NEAT1/EGR1 axis as well as its downstream effector RNA binding motif protein 25 (RBM25) in cerebral IR injury. Oxygen-glucose deprivation/reperfusion (OGD/R) and middle cerebral artery occlusion (MCAO) were used to establish in vitro and in vivo models of cerebral IR injury, respectively. According to our data, NEAT1, EGR1, and RBM25 levels were elevated in OGD/R-exposed SK-N-SH and SH-SY5Y cells and cerebral cortex of MCAO mice. NEAT1, EGR1, or RBM25 knockdown effectively reduced infarct volumes and apoptosis, and improved neurological function. Mechanistically, NEAT1 directly interacted with EGR1, which restrained WW domain containing E3 ubiquitin protein ligase 1 (WWP1)-mediated ubiquitination of EGR1 and subsequently caused EGR1 accumulation. EGR1 bound to RBM25 promoter and transcriptionally activated RBM25. Rescue experiments indicated that RBM25 overexpression abolished the therapeutic effects of NEAT1 knockdown. In conclusion, this work identified a novel NEAT1/EGR1/RBM25 axis in potentiating brain injury after IR insults, suggesting a potential therapeutic target for ischemic stroke.

Olfactory Impairment and Hippocampal Volume in a Chinese MCI Clinical Sample.

PURPOSE: The aim of this study was to evaluate the relationship between olfactory function and hippocampal volume in patients with mild cognitive impairment (MCI). METHODS: We enrolled a total of 31 MCI patients and 9 normal control subjects. All participants underwent 3.0 T-magnetic resonance imaging scanning. The scan results were processed using GE ADW4.6 processing software and V0xar 3D workstation to acquire the hippocampal volume. The University of Pennsylvania Smell Identification Test (UPSIT) was used to evaluate the olfactory function of MCI patients. The correlations of UPSIT score with hippocampal volume and hippocampal head volume were evaluated by Pearson correlation coefficient analysis. RESULTS: MCI patients had significantly smaller left (2.78±0.50 vs. 3.19±0.31 cm(3)) and right (2.97±0.42 vs. 3.31±0.25 cm(3)) hippocampal volumes compared with normal controls (P<0.05). In addition, patients with olfactory dysfunction had smaller volumes of the hippocampus (left hippocampal volume, 2.57±0.39 vs. 3.23±0.40 cm(3); right hippocampal volume, 2.86±0.43 vs. 3.22±0.30 cm(3)) and hippocampal head (left hippocampal head volume, 1.18±0.16 vs. 1.53±0.25 cm(3); right hippocampal head volume, 1.25±0.22 vs. 1.54±0.22 cm(3)) compared with those with normal olfactory function (P<0.05). No significant difference in the hippocampal body volume and hippocampal tail volume was found between MCI patients with olfactory loss and those with normal olfactory function. The UPSIT score was significantly positively correlated with left hippocampal volume (r=0.55, P<0.05), right hippocampal volume (r=0.42, P<0.05), left hippocampal head volume (r=0.53, P<0.05), and right hippocampal head volume (r=0.45, P<0.05). CONCLUSIONS: Olfactory function correlates well with hippocampal volume among patients with MCI.

The complete mitochondrial genome of the Thymallus grubii (Amur grayling).

In this study, we reported the complete sequence of mitochondrial genome of Thymallus grubii. The complete mitochondrial genome sequence was determined to be 16,662 bp in length and contain 13 protein-coding genes, 22 tRNA genes, 2 ribosomal genes, the control region and the origin of light-strand replication. In control region, only four CSBs (CSB-1, CSB-2, CSB-3 and CSB-F) were identified.

Effect of focal mild hypothermia on expression of MMP-9, TIMP-1, Tau-1 and ß-APP in rats with cerebral ischaemia/reperfusion injury.

PRIMARY OBJECTIVE: Following stroke, hypothermia is reported to reduce both cellular and extracellular damage. This study aimed to examine the effects of focal mild hypothermia on proteins associated with both extracellular (matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of MMP-9 (TIMP-1)) and cellular damage (Tau-1 and ß-amyloid precursor protein (ß-APP)) to characterize the protective effects of hypothermia. METHODS AND PROCEDURES: Male Wistar rats received ischaemic damage using a transient, focal ischaemia/reperfusion model. Afterwards, one group (HT) received 6 hours of focal mild hypothermia (33 °C) applied to the head, while another remained at normal temperature (NT). The brains were collected at 6, 12, 24, 48 and 72 hours after hypothermia to measure infarct volume ratio and to detect cells immunopositive for MMP-9, TIMP-1, Tau-1 and ß-APP, while neurological deficits were examined separately after 2 weeks. MAIN OUTCOMES AND RESULTS: Focal mild hypothermia had no effect on infarct volume ratio but expression of MMP-9, TIMP-1 Tau-1 and ß-APP was decreased. Furthermore, neurological function in the HT group was better than in the NT group. CONCLUSIONS: Focal mild hypothermia has protective effects on cerebral ischaemia-reperfusion injury characterized by decreased expression of MMP-9, TIMP-1, Tau-1 and ß-APP, along with improvement of neurological function despite no changes in infarct volume.