Association between Serum Magnesium Levels and Risk of Acute Kidney Injury in Patients with Traumatic Brain Injury: A Retrospective Cohort Study from the MIMIC-IV Database.

INTRODUCTION: The occurrence of acute kidney injury (AKI) is associated with a higher risk of mortality in patients with traumatic brain injury (TBI). This study aimed to explore the relationship between serum magnesium levels and the risk of AKI in patients with TBI. METHODS: Patients with TBI were identified from the Medical Information Mart Intensive Care IV (MIMIC-IV) 2008-2019. The relationship between serum magnesium levels at admission and magnesium coefficient of variation (CV) during hospitalization and the risk of AKI was analyzed using multivariable logistic regression analysis and expressed as odds ratio (OR) and 95% confidence interval (CI). Subgroup analyses were performed according to Glasgow Coma Scale (GCS) score (<14, ≥14), sepsis (no, yes), and estimated glomerular filtration rate (eGFR; <60, ≥60). RESULTS: Of the 991 patients included, 140 (14.13%) developed AKI during hospitalization. Patients with magnesium levels ≤1.7 mg/dL (tertile 1) (OR = 1.68, 95% CI: 1.01-2.81) were associated with a higher risk of AKI compared to those with magnesium levels of 1.7-2.0 mg/dL (tertile 2), but no association was found in those with magnesium levels >2.0 mg/dL (tertile 3) (p = 0.479). For magnesium CV, patients with magnesium CV >10% (tertile 3) (OR = 2.26, 95% CI: 1.16-4.41) were linked to an increased risk of AKI compared to those with magnesium CV ≤4% (tertile 1), but there may be a slight association between magnesium CV of 4%-10% (tertile 2) and AKI risk (OR = 1.86, 95% CI: 0.99-3.48; p = 0.053). Subgroup analyses showed that lower magnesium levels (≤1.7 mg/dL) or greater magnesium CV (>10%) were associated with a higher risk of AKI only in patients with a GCS score ≥14, non-sepsis, or eGFR ≥60 mL/min/1.73 m2 (p < 0.05). CONCLUSION: Lower serum magnesium levels at admission or greater magnesium CV during hospitalization were associated with a higher risk of AKI in patients with TBI.

Association of dietary fatty acid intake with hypertension in children and adolescents: evidence from the NHANES 2005-2018.

Aim: This study aims to evaluate the association between dietary fatty acid intake and hypertension in children and adolescents. Methods: This cross-sectional study used data of children and adolescents aged 8-17 years from the National Health and Nutrition Examination Survey (NHANES) 2005-2018. Dietary intake of total fat and fatty acid was evaluated via two 24-h dietary recall interviews. Multivariate logistic regression models were used to assess the association between fatty acid intake and hypertension, with odds ratios (ORs) and 95% confidence intervals (CIs) calculated. A subgroup analysis was conducted according to gender, age, and body mass index Z-score. Results: This study included 13,330 subjects, of which 11,614 were non-hypertensive and 1,716 were hypertensive. Higher intake of total polyunsaturated fatty acids (PUFAs) was associated with significantly lower odds of hypertension (OR = 0.85, 95% CI: 0.74-0.97, P = 0.018). No significant associations were found between the density of total saturated fatty acid, monounsaturated fatty acids, and PUFAs and the odds of hypertension (all P > 0.05). Increased intake of omega-3 (OR = 0.82, 95% CI: 0.72-0.93, P = 0.002) and omega-6 (OR = 0.86, 95% CI: 0.75-0.98, P = 0.025) PUFAs, octadecatrienoic acid (OR = 0.82, 95% CI: 0.72-0.93, P = 0.003), and octadecadienoic acid (OR = 0.86, 95% CI: 0.75-0.98, P = 0.025) was associated with significantly lower odds of hypertension, and individuals with higher omega-6/omega-3 ratio had significantly higher odds of hypertension (OR = 1.09, 95% CI: 1.02-1.17, P = 0.025). The density of omega-3 PUFAs (OR = 0.86, 95% CI: 0.78-0.95, P = 0.004) and octadecatrienoic acid (OR = 0.87, 95% CI: 0.78-0.96, P = 0.006) was inversely associated with the odds of hypertension, and the omega-6/omega-3 ratio was positively associated with the odds of hypertension (OR = 1.09, 95% CI: 1.02-1.17, P = 0.012). Conclusion: Total PUFA intake was negatively associated with the odds of hypertension in children and adolescents. Higher intake of omega-3 and omega-6 PUFAs, octadecatrienoic acid, and octadecadienoic acid, as well as density of omega-3 PUFAs and octadecatrienoic acid, was associated with lower odds of hypertension.

Effect of Gastrodin on Early Brain Injury and Neurological Outcome After Subarachnoid Hemorrhage in Rats.

Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage (SAH) remains unclear. In this study, we showed that intraperitoneal administration of gastrodin (100 mg/kg per day) significantly attenuated the SAH-induced neurological deficit, brain edema, and increased blood-brain barrier permeability in rats. Meanwhile, gastrodin treatment significantly reduced the SAH-induced elevation of glutamate concentration in the cerebrospinal fluid and the intracellular Ca2+ overload. Moreover, gastrodin suppressed the SAH-induced microglial activation, astrocyte activation, and neuronal apoptosis. Mechanistically, gastrodin significantly reduced the oxidative stress and inflammatory response, up-regulated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, phospho-Akt and B-cell lymphoma 2, and down-regulated the expression of BCL2-associated X protein and cleaved caspase-3. Our results suggested that the administration of gastrodin provides neuroprotection against early brain injury after experimental SAH.

Upregulated miRNA-622 inhibited cell proliferation, motility, and invasion via repressing Kirsten rat sarcoma in glioblastoma.

Glioblastoma has been reported as one of the leading causes of cancer-related death, and some factors including oncogenic genes and environments are involved in tumorigenesis. MicroRNAs (miRNAs) act as a kind of small and noncoding RNA, which can target the downstream molecules. Emerging reports demonstrate that microRNAs regulate the initiation and progression of different cancers. In the present study, we conducted in vitro experiment as well as clinical studies in a cohort of 20 glioblastoma samples. We demonstrated that miR-622 expression was lower in tumor tissues and cells, when compared to normal brain tissues and normal human astrocyte (NHA) cells, while K-Ras messenger RNA (mRNA) and protein showed the opposite expression profile. Overexpression of miR-622 suppressed tumor cell proliferation, migration, and invasion of A172, U87, and U251 cells. Accordingly, the proliferating cell nuclear antigen (PCNA), matrix metallopeptidase 2 (MMP2), and MMP9 expressions were also decreased due to miR-622 overexpression. Importantly, we discovered that wild Kirsten rat sarcoma (K-Ras) was a direct target of miR-622, which decreased the expression of K-Ras protein in A172, U87, and U251 cells. In conclusion, upregulated miRNA-622 inhibited cell proliferation, migration, and invasion via repressing K-Ras in the progression of glioblastoma, and miR-622-K-Ras pathway can be recommended as a potential target for treatment of glioblastoma.