The role of magnesium in cardiac arrest.

Cardiac arrest is a leading cause of death globally. Only 25.8% of in-hospital and 33.5% of out-of-hospital individuals who achieve spontaneous circulation following cardiac arrest survive to leave the hospital. Respiratory failure and acute coronary syndrome are the two most common etiologies of cardiac arrest. Effort has been made to improve the outcomes of individuals resuscitated from cardiac arrest. Magnesium is an ion that is critical to the function of all cells and organs. It is often overlooked in everyday clinical practice. At present, there have only been a small number of reviews discussing the role of magnesium in cardiac arrest. In this review, for the first time, we provide a comprehensive overview of magnesium research in cardiac arrest focusing on the effects of magnesium on the occurrence and prognosis of cardiac arrest, as well as in the two main diseases causing cardiac arrest, respiratory failure and acute coronary syndrome. The current findings support the view that magnesium disorder is associated with increased risk of cardiac arrest as well as respiratory failure and acute coronary syndrome.

The predictive value of eGFR combined with BNP detection in acute kidney injury after acute myocardial infarction.

Objective: The combined detection of eGFR and BNP may provide some value in predicting the occurrence of AKI after AMI, and the study is designed to propose and validate this hypothesis. Methods: In retrospective research, AMI patients hospitalized at Weifang People's Hospital from January to December 2020 were included. Whether AKI occurred within a week of admission, patients were divided into two groups. Clinical data from two groups of patients were collected, and the Logistic regression model analysed the risk factors for AKI after AMI. The association between eGFR and BNP was analysed using Pearson linear correlation. The predictive value of eGFR and BNP alone and combined detection on AKI after AMI was analysed using the receiver operating characteristic (ROC) curve. Results: Multivariate logistic regression showed that eGFR, BNP, HDLC, UA, and K ions were AKI risk factors (P < 0.05). The eGFR correlates negatively with BNP (R = -0.324, P < 0.05). The area under the curve (AUC) of eGFR and BNP alone and combined prediction for post-AMI AKI were 0.793, 0.826, and 0.831, respectively. Conclusion: The combined detection of eGFR and BNP has a high predictive value for AKI development in AMI patients.

Mediation of the APOE Associations With Cognition Through Cerebral Blood Flow: The CIBL Study.

Background: The ε4 allele of the apolipoprotein E (APOE) gene is a strong genetic risk factor for aging-related cognitive decline. However, the causal connection between ε4 alleles and cognition is not well understood. The objective of this study was to identify the roles of cerebral blood flow (CBF) in cognitive-related brain areas in mediating the associations of APOE with cognition. Methods: The multiple linear regression analyses were conducted on 369 subjects (mean age of 68.8 years; 62.9% of women; 29.3% of APOE ε4 allele carriers). Causal mediation analyses with 5,000 bootstrapped iterations were conducted to explore the mediation effects. Result: APOE ε4 allele was negatively associated with cognition (P < 0.05) and CBF in the amygdala, hippocampus, middle temporal gyrus, posterior cingulate, and precuneus (all P < 0.05). The effect of the APOE genotype on cognition was partly mediated by the above CBF (all P < 0.05). Conclusion: CBF partially mediates the potential links between APOE genotype and cognition. Overall, the APOE ε4 allele may lead to a dysregulation of the vascular structure and function with reduced cerebral perfusion, which in turn leads to cognitive impairment.

Correlation between dietary selenium intake and stroke in the National Health and Nutrition Examination Survey 2003-2018.

BACKGROUND: Epidemiologic evidence of the effect of dietary selenium intake on stroke risk remains controversial. This study aimed to examine the cross-sectional correlation between dietary selenium intake and the risk of stroke in adults. MATERIALS AND METHODS: We retrospectively analysed 39,438 participants from the National Health and Nutrition Examination Survey 2003-2018, aged 20-85 years. Participants were divided into quartiles depending on daily dietary selenium intake: quartile 1 (0-77 µg), quartile 2 (77-108 µg), quartile 3 (108-148 µg), and quartile 4 (148-400 µg). The dose-response relationship was assessed using the restricted cubic spline function. RESULTS: The adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of stroke were 0.70 (0.55, 0.88) for participants in quartile 2, 0.71 (0.53, 0.93) for quartile 3, and 0.61 (0.43, 0.85) for quartile 4 compared with that in quartile 1. p-Value for trend through quartiles was .007. A non-linear negative correlation between dietary selenium intake and stroke was observed in the threshold effect analysis and restricted cubic spline function (p-value for non-linearity < .001). An initial decrease in odds of stroke lower than 105 µg/day selenium intake (0.61 [0.44, 0.85], p = .004) was followed by a platform beyond 105 µg/day (0.97 [0.81, 1.16], p = .723). In the subgroup analysis, adjusted ORs (95% CIs) of stroke were 0.51 (0.36, 0.70) for female participants, 0.63 (0.40, 0.99) for participants with age <60 years, 0.63 (0.47, 0.85) for participants with poverty-income ratio < 2.14, 0.66 (0.50, 0.87) for participants with overweight and obesity, 0.66 (0.52, 0.84) for participants with hypertension, 0.72 (0.53, 0.97) for participants without diabetes, and 0.72 (0.56, 0.92) for non-anaemic participants. CONCLUSIONS: Dietary selenium had a negative and non-linear correlation with the risk of stroke in adults. The correlation varied across different population subgroups.KEY MESSAGESDietary selenium had a negative and non-linear correlation with the risk of stroke in adults.Non-linear negative correlation trends were observed in subpopulations of females, age <60 years, poverty-income ratio <2.14, overweight and obesity, hypertension, non-diabetes, and non-anaemia.Dietary selenium intake of approximately 105 µg per day has an optimum effect on stroke.

Association of migraine with patent foramen ovale closure: A systematic review and meta-analysis.

Background: The potential correlation between patent foramen ovale (PFO) and migraine has been previously reported, but whether PFO closure plays a role in reducing migraine burden has not reached an agreement. Method: We searched PubMed, Embase, China National Knowledge Infrastructure (CNKI), Wanfang Database, VIP Science Technology Periodical Database and China Biology Medicine Database (CBM) through September 30, 2021 to identify associations between PFO closure and outcome of migraine burden. The control groups consisted of drug treatment or sham procedure. Result: Three randomized clinical trials (RCT) and 9 case-control studies were eligible for inclusion (1754 participants), of which 7 reported nonrecurrence of migraine, 4 reported reduced migraine-frequency and migraine-days, and 5 reported HIT-6 score and 4 reported MIDAS score. The mean (SD) age of participants was 40.68 (3.81) years and 1340 (76.39%) were women. PFO closure was significantly associated with a reduced risk of migraine-recurrence by 4.47 (95% CI, 2.94-6.80; I2 = 12%), frequency of migraine by 0.35 (95% CI, 0.17-0.53; I2 = 0%) and monthly migraine days by 0.28 (95% CI, 0.10-0.46), and decreased score of HIT-6 (SMD 1.23, 95 %CI 0.52-1.95, I2 = 93%). Conclusion: Transcatheter PFO closure is significantly associated with burden reduction of migraine headache.

Recent Advances in Basic Research for CSF1R-Microglial Encephalopathy.

Colony-stimulating factor-1 receptor-microglial encephalopathy is a rare rapidly progressive dementia resulting from colony-stimulating factor-1 receptor (CSF1R) mutations, also named pigmentary orthochromatic leukodystrophy (POLD), hereditary diffuse leukoencephalopathy with spheroids (HDLS), adult-onset leukoencephalopathy with axonal spheroids, and pigmented glia (ALSP) and CSF1R-related leukoencephalopathy. CSF1R is primarily expressed in microglia and mutations normally directly lead to changes in microglial number and function. Many animal models have been constructed to explore pathogenic mechanisms and potential therapeutic strategies, including zebrafish, mice, and rat models which are with CSF1R monogenic mutation, biallelic or tri-allelic deletion, or CSF1R-null. Although there is no cure for patients with CSF1R-microglial encephalopathy, microglial replacement therapy has become a topical research area. This review summarizes CSF1R-related pathogenetic mutation sites and mechanisms, especially the feasibility of the microglia-original immunotherapy.

Plasma p-tau181 Level Predicts Neurodegeneration and Progression to Alzheimer's Dementia: A Longitudinal Study.

Background: Plasma-based biomarkers would be potential biomarkers for early diagnosis of Alzheimer's disease (AD) because they are more available and cost-effective than cerebrospinal fluid (CSF) or neuroimaging. Therefore, we aimed to evaluate whether phosphorylated tau181 (p-tau181) in plasma could be an accurate AD predictor. Methods: Participants from the ADNI database included 185 cognitively unimpaired subjects with negative Aß (CU-), 66 subjects with pre-clinical AD (CU with positive Aß), 164 subjects with mild cognitive impairment with negative Aß (MCI-), 254 subjects with prodromal AD (MCI with positive Aß), and 98 subjects with dementia. Multiple linear regression models, linear mixed-effects models, and local regression were used to explore cross-sectional and longitudinal associations of plasma p-tau181 with cognition, neuroimaging, or CSF biomarkers adjusted for age, sex, education, and APOE genotype. Besides, Kaplan-Meier and adjusted Cox-regression model were performed to predict the risk of progression to dementia. Receiver operating characteristic analyses were performed to evaluate the predictive value of p-tau181. Results: Plasma p-tau181 level was highest in AD dementia, followed by prodromal AD and pre-clinical AD. In pre-clinical AD, plasma p-tau181 was negatively associated with hippocampal volume (ß = -0.031, p-value = 0.017). In prodromal AD, plasma p-tau181 was associated with decreased global cognition, executive function, memory, language, and visuospatial functioning (ß range -0.119 to -0.273, p-value < 0.05) and correlated with hippocampal volume (ß = -0.028, p-value < 0.005) and white matter hyperintensity volume (WMH) volume (ß = 0.02, p-value = 0.01). In AD dementia, increased plasma p-tau181 was associated with worse memory. In the whole group, baseline plasma p-tau181 was significantly associated with longitudinal increases in multiple neuropsychological test z-scores and correlated with AD-related CSF biomarkers and hippocampal volume (p-value < 0.05). Meanwhile, CU or MCI with high plasma p-tau181 carried a higher risk of progression to dementia. The area under the curve (AUC) of the adjusted model (age, sex, education, APOE genotype, and plasma p-tau181) was 0.78; that of additionally included CSF biomarkers was 0.84. Conclusions: Plasma p-tau181 level is related to multiple AD-associated cognitive domains and AD-related CSF biomarkers at the clinical stages of AD. Moreover, plasma p-tau181 level is related to the change rates of cognitive decline and hippocampal atrophy. Thus, this study confirms the utility of plasma p-tau181 as a non-invasive biomarker for early detection and prediction of AD.