Isolated unilateral brachial plexus injury following carbon monoxide intoxication: a case report and literature review.

Carbon monoxide (CO) is a gas that has no odor or color, making it difficult to detect until exposure leads to coma or death. CO poisoning is one of the most common and deadly poisonings around the world. CO poisoning is a common and often fatal form of poisoning worldwide. A toxic effect of CO is tissue hypoxia, which leads to systemic complications. Additionally, there may be severe neurological symptoms and delayed complications following CO poisoning. However, peripheral neuropathy is relatively rare after CO poisoning. Previously, only one case of unilateral plexopathy after CO poisoning, accompanied by rhabdomyolysis and cognitive dysfunction, has been reported. In this report, an isolated unilateral brachial plexopathy following CO intoxication is described. A key mechanism in this case may be CO-induced spinal cord ischemia. Immediate administration of hyperbaric oxygen therapy (HBOT) is crucial to prevent peripheral neuropathy after acute CO intoxication. Hyperbaric oxygen therapy (HBOT) should be administered immediately after acute CO intoxication to prevent peripheral neuropathy. Additionally, peripheral neuropathy following acute CO intoxication may benefit from consistent rehabilitation training.

Microglia in brain aging: An overview of recent basic science and clinical research developments.

Aging is characterized by progressive degeneration of tissues and organs, and it is positively associated with an increased mortality rate. The brain, as one of the most significantly affected organs, experiences age-related changes, including abnormal neuronal activity, dysfunctional calcium homeostasis, dysregulated mitochondrial function, and increased levels of reactive oxygen species. These changes collectively contribute to cognitive deterioration. Aging is also a key risk factor for neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. For many years, neurodegenerative disease investigations have primarily focused on neurons, with less attention given to microglial cells. However, recently, microglial homeostasis has emerged as an important mediator in neurological disease pathogenesis. Here, we provide an overview of brain aging from the perspective of the microglia. In doing so, we present the current knowledge on the correlation between brain aging and the microglia, summarize recent progress of investigations about the microglia in normal aging, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, and then discuss the correlation between the senescent microglia and the brain, which will culminate with a presentation of the molecular complexity involved in the microglia in brain aging with suggestions for healthy aging.

The Apelin/APJ system modulates seizure activity and endocytosis of the NMDA receptor GluN2B subunit.

In the central nervous system (CNS), the apelin/APJ system is broadly expressed. According to some studies, activation of this system protects against excitotoxicity mediated by N-methyl-D-aspartate (NMDA) receptors and exerts neuroprotective effects. However, the role of this system in epilepsy remains unclear. In the present study, immunofluorescence staining and western blotting were used to assess APJ localization and expression in the brains of mice with recurrent spontaneous seizures induced by kainic acid (KA). Behavior and local field potentials (LFPs) were assessed in mice with KA-induced seizures. Susceptibility to seizures was assessed in a pentylenetetrazole (PTZ)-induced seizure model. Whole-cell patch-clamp recordings were used to evaluate the role of the apelin/APJ system in regulating synaptic transmission in brain slices from mice in which Mg2+-free medium was used to induce seizures. NMDA receptor GluN2B subunit expression and phosphorylation of GluN2B at Ser1480 were measured in the mouse hippocampus. APJ was primarily localized in neurons, and its expression was upregulated in the epileptic brain. APJ activation after KA-induced status epilepticus (SE) reduced epileptic activity, whereas APJ inhibition aggravated epileptic activity. In the PTZ model, APJ activation reduced and APJ inhibition increased susceptibility to seizures. The apelin/APJ system affected NMDA receptor-mediated postsynaptic currents in patch-clamp recordings. Moreover, APJ regulated the levels of GluN2B phosphorylated at Ser1480 and the abundance of cell-surface GluN2B in neurons. Furthermore, endocytosis of the NMDA receptor GluN2B subunit was regulated by the apelin/APJ system. Together, our findings indicate that the apelin/APJ system modulates seizure activity and may be a novel therapeutic target for epilepsy.

Long-term intermittent fasting improves neurological function by promoting angiogenesis after cerebral ischemia via growth differentiation factor 11 signaling activation.

Intermittent fasting (IF), an alternative to caloric restriction, is a form of time restricted eating. IF conditioning has been suggested to have neuroprotective effects and potential long-term brain health benefits. But the mechanism underlying remains unclear. The present study focused on the cerebral angiogenesis effect of IF on ischemic rats. Using a rat middle cerebral artery occlusion model, we assessed neurological outcomes and various vascular parameters such as microvessel density (MVD), regional cerebral blood flow (rCBF), proliferation of endothelial cells (ECs), and functional vessels in the peri-infarct area. IF conditioning ameliorated the modified neurological severity score and adhesive removal test, increased MVD, and activated growth differentiation factor 11 (GDF11)/activin-like kinase 5 (ALK5) pathways in a time-dependent manner. In addition, long-term IF conditioning stimulated proliferation of ECs, promoted rCBF, and upregulated the total vessel surface area as well as the number of microvessel branch points through GDF11/ALK5 pathways. These data suggest that long-term IF conditioning improves neurological outcomes after cerebral ischemia, and that this positive effect is mediated partly by angiogenesis in the peri-infarct area and improvement of functional perfusion microvessels in part by activating the GDF11/ALK5 signaling pathway.

Influence of Citric Acid on the Fundamental Properties of CO2 Cured Magnesium Oxysulfate Paste.

Magnesium oxysulfate (MOS), mainly composed of magnesium oxide and magnesium sulfate, is a kind of gas-hardening cementing material with low energy consumption and CO2 emissions. In order to develop environment-friendly cement-based materials, MOS needs to be studied systematically. The paper mainly investigates the influence of citric acid (a retarder) on the working and mechanical properties of MOS paste. In this study, the setting time of fresh MOS paste is determined. The flexural and compressive strengths of hardened specimens exposed to the environment of water dry-wet (D-W) alternations, freeze-thaw (F-T) cycles, and sulfate D-W alternations are investigated. Furthermore, the drying shrinkage (D-S) rate of MOS paste is tested for 3 days and 28 days. The specimens are cured in standard or CO2 curing environments. A scanning electron microscope energy spectrum (SEM-EDS) is obtained to analyze the morphology of hydration products. Results show that citric acid can increase the setting time of MOS paste. The citric acid and CO2 curing have a positive effect on the mechanical strengths and the resistance to erosion by water, F-T cycles, and sulfate D-W alternations. The D-S rate decreased in relation to the increasing dosages of citric acid and increased with CO2 curing. MOS with 0.3% of the total binder material mass shows the best erosion resistance. As observed in the results of SEM-EDS, the CO2 curing and the citric acid can make the hydration products denser.

Circulating Soluble CD163: A Potential Predictor for the Functional Outcome of Acute Ischemic Stroke.

Background: CD163 is a transmembrane glycoprotein receptor expressed on innate immune cells that sheds from the cell membrane and circulates as a soluble form (sCD163). This study aimed to investigate the circulating levels and clinical relevance of soluble CD163 (sCD163) in acute ischemic stroke (AIS). Methods: This study recruited 300 patients with AIS and 78 healthy controls. The patients were followed up for 1 month to observe the functional outcomes. The neurological functions of the patients were assessed using the NIH Stroke Scale (NIHSS) and the modified Rankin Scale (mRS). The plasma concentrations of sCD163 at the baseline (patient admission) were determined by ELISA. Results: We found that patients with AIS had significantly higher plasma sCD163 concentrations than the healthy control. Patients with high sCD163 concentrations had better functional outcomes than patients with low sCD163 concentrations. The plasma sCD163 concentrations were positively associated with the NIHSS scores and infarction volume at the baseline. The plasma sCD163 was positively associated with the improvement of the NIHSS scores but was negatively associated with the risk of poor functional outcomes during follow-up. Conclusions: These findings indicate that circulating sCD163 is a potential biomarker that is associated with disease severity and the functional outcome of AIS.

Effects of mesencephalic astrocyte-derived neurotrophic factor on cerebral angiogenesis in a rat model of cerebral ischemia.

Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum stress-related protein that exhibits neuroprotective effects. Recent studies have shown that MANF promotes poststroke functional recovery in rats. However, the underlying mechanisms have not yet been fully understood. Here, we examined the effects of MANF on cerebral angiogenesis in a permanent middle cerebral artery occlusion model in rats. Recombinant human MANF was administered intracerebroventricularly 24 h after stroke. We performed neurobehavioral tests and assessed microvessel density, functional microvessels, and regional cerebral blood flow (rCBF), as well as detected angiogenic factors in the peri-infarct cerebral cortex. Results showed that MANF ameliorated neurobehavioral scores, promoted rCBF, upregulated the expression of CD34, as well as the total vessel surface area and the number of microvessel branch points, and activated the vascular endothelial growth factor (VEGF) pathway. In conclusion, our findings provide insight into the mechanisms of MANF in promoting functional recovery from ischemic stroke. Our results suggest that MANF improves neurobehavioral recovery from cerebral ischemic injury, and that this effect is mediated partly by its proangiogenic effects and augmentation of rCBF, which are possibly associated with VEGF.

Detection of cardioembolic stroke with B-type natriuretic peptide or N-terminal pro-BNP: a comparative diagnostic meta-analysis.

Background: B-type natriuretic peptides (BNPs) have shown promise in detecting cardioembolic stroke. However, there has been little investigation comparing the diagnostic efficacy of BNP and its cleavage by-product N-terminal peptide (NT-proBNP) in cardioembolic stroke patients. Therefore, the aim of this meta-analysis will be to comparatively assess the diagnostic efficacy of BNP versus NT-proBNP in distinguishing cardioembolic stroke from non-cardioembolic stroke in adult ischemic stroke patients. Methods: We conducted a literature search of several databases for prospective studies assessing the use of BNP or NT-proBNP to detect cardioembolic stroke in adult acute ischemic stroke patients. Only clinical studies reporting the diagnostic performance of BNP or NT-proBNP in predicting cardioembolic stroke in adult ischemic stroke patients were included. Diagnostic performance outcomes were summarized using forest plots and summary receiver operating characteristic (SROC) curves. Results: Ten BNP prospective cohort studies and six NT-proBNP prospective cohort studies were finally included in the meta-analysis. BNP showed a summary sensitivity of 0.65 (95% confidence interval (CI): 0.63-0.68), a summary specificity of 0.85 (95% CI: 0.83-0.87), and an area under the SROC curve of 0.8718 (standard error (SE): 0.0248). NT-proBNP showed a summary sensitivity of 0.55 (95% CI: 0.52-0.59), a summary specificity of 0.93 (95% CI: 0.91-0.94), and an AUC of 0.8746 (SE: 0.0280). Discussion: BNP and NT-proBNP display closely equivalent overall diagnostic accuracies in distinguishing cardioembolic stroke from non-cardioembolic stroke in adult ischemic stroke patients, with BNP showing a superior sensitivity and NT-proBNP showing a superior specificity.