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.

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.

Single-nucleus RNA sequencing reveals that macrophages and smooth muscle cells promote carotid atherosclerosis progression through mitochondrial autophagy.

Carotid atherosclerotic plaques are the manifestation of atherosclerosis in the carotid arteries and can significantly increase the incidence of cerebrovascular disease. Macrophages and smooth muscle cells are crucial for their development. To reveal the mechanism of carotid atherosclerotic plaque formation, we performed single-nucleus RNA sequencing of the carotid plaque tissue and identified 11 cell types, and the macrophages were divided into 5 different macrophage subpopulations. The macrophages and smooth muscle cells in the patients with symptomatic carotid atherosclerotic plaques caused intraplaque cell death via the mitochondrial autophagic pathway, resulting in plaque instability and rupture, which in turn led to clinical cardiovascular and cerebrovascular events. The findings provide new insights into carotid atherosclerosis formation, and this may provide new directions for the prevention and treatment of carotid atherosclerosis.

Repeated intracerebral hemorrhage after craniotomy for a distal middle cerebral artery aneurysm: A case report.

RATIONALE: Distal middle cerebral artery aneurysms are very rare in the clinic, and craniotomy clipping is the better treatment after diagnosis. However, patients can also have repeated acute intracerebral hemorrhage after craniotomy for aneurysm, which has not been previously reported. PATIENT CONCERNS: A 24-year-old male patient was admitted to our hospital with headache, nausea, and vomiting. He was well before, had no family history of cerebrovascular disease or hypertension, and had no history of trauma. DIAGNOSES: Computer tomography and digital subtraction angiography of the brain revealed intracranial hematoma and an aneurysm located at the M4 segment of the left middle cerebral artery. INTERVENTIONS: The patient underwent 2 surgeries to treat the aneurysm, followed by 2 operations for acute cerebral hemorrhage. OUTCOMES: Despite repeated surgical treatments, the patient had a poor prognosis and eventually died of respiratory and circulatory failure after repeated brain bleeding. LESSONS: Briefly, it is of great importance to consider the risk factors of cerebral hemorrhage, and provide individualized treatment and psychological counseling for patients with intracerebral hemorrhage.

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.

Diagnostic value of 3D time-of-flight MRA in trigeminal neuralgia.

The aim of this meta-analysis was to evaluate the diagnostic value of 3D time-of-flight magnetic resonance angiography (3D-TOF-MRA) in trigeminal neuralgia (TN). Relevant studies were identified by computerized database searches supplemented by manual search strategies. The studies were included in accordance with stringent inclusion and exclusion criteria. Following a multistep screening process, high quality studies related to the diagnostic value of 3D-TOF-MRA in TN were selected for meta-analysis. Statistical analyses were conducted using Statistical Analysis Software (version 8.2; SAS Institute, Cary, NC, USA) and Meta Disc (version 1.4; Unit of Clinical Biostatistics, Ramon y Cajal Hospital, Madrid, Spain). For the present meta-analysis, we initially retrieved 95 studies from database searches. A total of 13 studies were eventually enrolled containing a combined total of 1084 TN patients. The meta-analysis results demonstrated that the sensitivity and specificity of the diagnostic value of 3D-TOF-MRA in TN were 95% (95% confidence interval [CI] 0.93-0.96) and 77% (95% CI 0.66-0.86), respectively. The pooled positive likelihood ratio and negative likelihood ratio were 2.72 (95% CI 1.81-4.09) and 0.08 (95% CI 0.06-0.12), respectively. The pooled diagnostic odds ratio of 3D-TOF-MRA in TN was 52.92 (95% CI 26.39-106.11), and the corresponding area under the curve in the summary receiver operating characteristic curve based on the 3D-TOF-MRA diagnostic image of observers was 0.9695 (standard error 0.0165). Our results suggest that 3D-TOF-MRA has excellent sensitivity and specificity as a diagnostic tool for TN, and that it can accurately identify neurovascular compression in TN patients.