The mechanism of hypoxia-inducible factor-1α enhancing the transcriptional activity of transferrin ferroportin 1 and regulating the Nrf2/HO-1 pathway in ferroptosis after cerebral ischemic injury.

Cerebral ischemic/reperfusion (I/R) injury has high disability and morbidity. Hypoxia-inducible factor-1α (HIF-1α) may enhance the transcriptional activity of transferrin ferroportin 1 (FPN1) in regulating ferroptosis after cerebral ischemia injury (CII). In this study, cerebral I/R injury rat models were established and treated with pcDNA3.

A novel PROTAC molecule dBET1 alleviates pathogenesis of experimental autoimmune encephalomyelitis in mice by degrading BRD4.

Neuroinflammation and neurodegeneration are hallmarks of multiple sclerosis (MS). Bromodomain-containing protein 4 (BRD4), a bromodomain and extra-terminal domain (BET) protein family member, is indispensable for the transcription of pro-inflammatory genes. Therefore, inhibiting BRD4 may be a prospective therapeutic approach for modulating the inflammatory response and regulating the course of MS.

Non-insulin-based insulin resistance indices predict early neurological deterioration in elderly and middle-aged acute ischemic stroke patients in Northeast China.

Insulin resistance (IR) has a strong association with acute ischemic stroke (AIS) occurrence and poor prognosis of afflicted patients. However, the relation between early neurological deterioration (END) risk and IR in elderly and middle-aged patients remains to be thoroughly studied. Here, we investigated the relationship between four indicators of IR and the risk of END in middle-aged patients patients with AIS.

Association of anion gap and albumin corrected anion gap with acute kidney injury in patients with acute ischemic stroke.

Background: Acute kidney injury (AKI) has become a common complication of acute ischemic stroke (AIS) and may have a significant impact on clinical outcomes. Anion gap (AG)/albumin corrected anion gap (ACAG) are used to assess acid-base balance status and help identify the severity of metabolic acidosis.

Objectives: To explore the association of AG and ACAG with the risk of AKI in AIS patients admitted to the intensive care unit (ICU).

Discovery and validation of Ferroptosis-related molecular patterns and immune characteristics in Alzheimer's disease.

Background: To date, the pathogenesis of Alzheimer's disease is still not fully elucidated. Much evidence suggests that Ferroptosis plays a crucial role in the pathogenesis of AD, but little is known about its molecular immunological mechanisms. Therefore, this study aims to comprehensively analyse and explore the molecular mechanisms and immunological features of Ferroptosis-related genes in the pathogenesis of AD.

Predictive values of systemic inflammatory responses index in early neurological deterioration in patients with acute ischemic stroke.

Background: Acute ischemic stroke (AIS) is the main cause of worldwide death and disability. Early neurological deterioration (END) can further increase the probability of death and disability in patients with ischemic stroke. Therefore, it is essential to find biomarkers to predict END early.

Extracellular vesicles from bone marrow stromal cells reduce the impact of stroke on glial cell activation and blood brain-barrier permeability via a putative miR-124/PRX1 signalling pathway.

Ischaemic stroke (IS) is a cerebrovascular disease caused by cerebral infarction and cerebral artery occlusion. In this study, we proposed that EVs from bone marrow stromal cells (BMSCs) could reduce the impact of stroke by reducing the resultant glial cell activation and blood-brain barrier (BBB) leak. We furthermore investigated some of the signalling mechanisms.

LncRNA Snhg8 attenuates microglial inflammation response and blood-brain barrier damage in ischemic stroke through regulating miR-425-5p mediated SIRT1/NF-κB signaling.

Increasing studies have indicated that abnormal expressed long noncoding RNAs (lncRNAs) play a vital role in ischemic stroke. Small nucleolar RNA host gene 8 (Snhg8), a member of lncRNAs, has been found to induce neuronal apoptosis in chronic cerebral ischemia models. Here, we aim to explore the function and molecular mechanism of Snhg8 in modulating microglial inflammation as well as brain microvascular endothelial cell (BMEC) damage following ischemic injury.

Electron-Transfer-Enhanced Cation-Cation Interactions in Homo- and Heterobimetallic Actinide Complexes: A Relativistic Density Functional Theory Study.

To provide deep insight into cation-cation interactions (CCIs) involving hexavalent actinyl species that are major components in spent nuclear fuel and pose important implications for the effective removal of radiotoxic pollutants in the environment, a series of homo- and heterobimetallic actinide complexes supported by cyclopentadienyl (Cp) and polypyrrolic macrocycle (HL) ligands were systematically investigated using relativistic density functional theory. The metal sort in both parts of (THF)(HL)(OAnO) and (An')Cp from U to Np to Pu, as well as the substituent bonding to Cp from electron-donating Me to H to electron-withdrawing Cl, SiH, and SiMe, was changed. Over 0.

NaCrCuWO.16HO induces apoptosis in human ovarian cancer SKOV3 cells through the p38 signaling pathway.

Ovarian carcinoma is a common malignant disease worldwide with a poor therapeutic response. The present study investigated the effects of NaCrCuWO.16HO (CrCuW) on ovarian cancer cell growth and investigated the mechanisms underlying its actions.

Astemizole protects against human umbilical vein endothelial cell injury induced by hydrogen peroxide via the p53 signaling pathway.

Astemizole has gained attention as an antineoplastic drug that targets important ion channels. The present study aimed to investigate the protective effects of astemizole against hydrogen peroxide (H2O2)‑induced oxidative damage to human umbilical vein endothelial cells (HUVECs). HUVECs were pretreated with astemizole (0.

The Dissection of Expression Quantitative Trait Locus Hotspots.

Studies of the genetic loci that contribute to variation in gene expression frequently identify loci with broad effects on gene expression: expression quantitative trait locus hotspots. We describe a set of exploratory graphical methods as well as a formal likelihood-based test for assessing whether a given hotspot is due to one or multiple polymorphisms. We first look at the pattern of effects of the locus on the expression traits that map to the locus: the direction of the effects and the degree of dominance.

Multivariate Boosting for Integrative Analysis of High-Dimensional Cancer Genomic Data.

In this paper, we propose a novel multivariate component-wise boosting method for fitting multivariate response regression models under the high-dimension, low sample size setting. Our method is motivated by modeling the association among different biological molecules based on multiple types of high-dimensional genomic data. Particularly, we are interested in two applications: studying the influence of DNA copy number alterations on RNA transcript levels and investigating the association between DNA methylation and gene expression.

Identification of the Bile Acid Transporter Slco1a6 as a Candidate Gene That Broadly Affects Gene Expression in Mouse Pancreatic Islets.

We surveyed gene expression in six tissues in an F2 intercross between mouse strains C57BL/6J (abbreviated B6) and BTBR T(+) tf/J (abbreviated BTBR) made genetically obese with the Leptin(ob) mutation. We identified a number of expression quantitative trait loci (eQTL) affecting the expression of numerous genes distal to the locus, called trans-eQTL hotspots. Some of these trans-eQTL hotspots showed effects in multiple tissues, whereas some were specific to a single tissue.

FMR1 CGG expansions: prevalence and sex ratios.

We have estimated the prevalence of FMR1 premutation and gray zone CGG repeat expansions in a population-based sample of 19,996 male and female adults in Wisconsin and compared the observed sex ratios of the prevalence of FMR1 CGG premutation and gray zone expansions to theoretical sex ratios. The female premutation prevalence was 1 in 148 and comparable to past research, but the male premutation prevalence of 1 in 290 is somewhat higher than most previous estimates. The female:male premutation prevalence ratio is in line with the theoretically predicted sex ratio.