The Association between Migraine and Fetal-Type Posterior Cerebral Artery in Patients with Ischemic Stroke.

OBJECTIVE: The aim of the study was to determine if migraine is associated with fetal-type posterior cerebral artery (PCA) in patients with ischemic stroke. METHOD: In this cross-sectional study, patients with acute ischemic stroke were enrolled from two hospitals. The history of migraine headache was evaluated during a face-to-face interview. The variants of fetal-type PCA were assessed with MRA, CTA, or DSA. Patients with and without migraine were compared in terms of fetal-type PCA status and other clinic characteristics. Multivariate logistic regression analyses were performed to adjust for confounders and provide risk estimates for observed associations. RESULT: In 750 patients qualified for analysis, 85 (11.3%) were determined with migraine. Patients with migraine had a higher proportion of female gender (51.8% vs. 31.0%, p < 0.001), hypertension (72.9% vs. 57.7%, p = 0.007), and fetal-type PCA (36.5% vs. 20.1%, p = 0.001), while lower proportion of current smoking (25.9% vs. 38.3%, p = 0.025) than patients without migraine. National Institutes of Health Stroke Scale (NIHSS) score (3 vs. 2, p = 0.016) was also higher in migraineurs than in non-migraineurs. After adjustment for confounders, fetal-type PCA status was independently associated with migraine (odds ratio [OR] = 2.06; 95% confidence interval [CI], 1.25-3.38; p = 0.005). Other factors associated to migraine included female gender (OR = 2.03; 95% CI, 1.13-3.62; p = 0.017), hypertension (OR = 1.97; 95% CI, 1.17-3.34; p = 0.011), and NIHSS score (OR = 1.08; 95% CI, 1.01-1.16; p = 0.018). CONCLUSION: Migraine was associated with fetal-type PCA in patients with ischemic stroke. This finding supported the hypothesis that vascular mechanisms get involved in the migraine-stroke association.

Combined exposure of PS-MPs with NaF induces Sertoli cell death and dysfunction via ferroptosis and apoptosis.

The individual toxicity of sodium fluoride (NaF) and microplastics (MPs) has been extensively documented. Owing to their high specific surface area, widespread presence and durability, MPs can adsorb a broad spectrum of environmental contaminants into the organism. However, the combined toxicity of NaF and MPs has not been investigated. This study aimed to assess the effects of combined exposure to NaF and MPs on the function of testicular Sertoli cells (SCs) in male mice, and to investigate the underlying molecular mechanisms. The study revealed that combined exposure to NaF and MPs resulted in a decrease in the negative surface charge of MPs, along with an increase in the number of MPs entering the SCs. Through in vivo observation of the testicular pathological structure, spermatogenesis, and cell apoptosis in 180-day-old male mice, we discovered that combined exposure to NaF (80 mg/L) and MPs (10 mg/L) heightened reproductive toxicity compared to the individual exposure groups. This was evidenced by testicular structural defects, impaired spermatogenesis, and increased testicular cell apoptosis. Our in vitro studies showed that NaF (21 µg/mL) and MPs (100 µg/mL) synergistically induced SCs apoptosis and ferroptosis, leading to a reduction in SCs number and dysfunction. This ultimately resulted in structural and functional damage to the testes. Our findings demonstrate, for the first time, the synergistic effects of NaF and MPs on reproductive toxicity in mammals. These insights may provide valuable contributions to co-toxicity studies involving MPs and other environmental pollutants.

[Effect of mild hypothermia on the expression of acid-sensing ion channels 1a and 2a following global cerebral ischemia-reperfusion in rats].

OBJECTIVE: To investigate the effects of mild hypothermia on the expression of ASIC1a and ASIC2a in the rat hippocampus following global cerebral ischemia-reperfusion, so as to speculate the underlying mechanisms of neuroresuscitation. METHODS: Ninety five male SD rats were randomly divided into five groups (n = 19): sham operation group (I), model group (II), mild hypothermia group (III), PcTX1 group (IV), mild hypothermia combined PcTX1 group (V). Transient (15 min) global cerebral ischemia was induced by the four-vessel occlusion. PcTX1 (500 ng/ml) 6 µl were injected into lateral cerebral ventricle immediately after reperfusion in group IV and V, while the equal volume of normal saline was injected into lateral cerebral ventricle immediately after reperfusion in the other three groups. At the same time, mild hypothermia after reperfusion was performed and lasted for 6 hours in group III and V, the rectal temperature was reduced to 32 - 33°C within 15 min, while it was maintained at 36 - 37°C by lamp in other three groups. Determination the expression of ASIC1a and ASIC2a protein at 6 h and 24 h of reperfusion, and the expression of ASIC1a and ASIC2a mRNA at 24 h of reperfusion. Observe the pathomorphological changes of hippocampal CA1 neurons at 24 h of reperfusion. Detect the brain water content at 72 h of reperfusion. RESULTS: The difference in the expression of ASIC1a mRNA and protein among the groups was not changed significantly (P > 0.05). Compared with group I, the expression of ASIC2a mRNA and ASIC2a protein was up-regulated in other groups (P < 0.05). It was significantly higher in group III and V than in group II and IV (P < 0.05). Compared to 6 h of reperfusion, the expression of ASIC2a protein was higher in group II, III, IV and V respectively after 24 h of reperfusion. Compared to group I, the number of pyramidal cells in CA1 region of hippocampus in group II, III, IV and V were decreased at 24 h of reperfusion (P < 0.01). Compared to group II, the number of pyramidal cells in CA1 region of hippocampus in group III, IV and V were increased at 24 h of reperfusion (P < 0.01); and compared to group III and IV, the number of pyramidal cells at 24 h of reperfusion in group V was significantly higher (P < 0.01). Compared to group I, the content of brain water in II, III and IV group were increased at 72 h of reperfusion (P < 0.01). Compared to group II, the content of brain water in group III, IV and V were decreased at 72 h of reperfusion (P < 0.01). Giving mild hypothermia or PcTX1 could alleviate the damage in CA1 region of hippocampus, with the best effect in group V, which administers PcTX1 combined mild hypothermia. CONCLUSION: Mild hypothermia attenuates global cerebral ischemia-reperfusion of rat, which may up-regulate the expression of ASIC2a mRNA and protein. Mild hypothermia combined by PcTX1 could induce neuroresuscitation.

Application of distant live broadcast in clinical anesthesiology teaching.

OBJECTIVE: To explore the application value and effect of distance live broadcast in Clinical Anesthesiology teaching. METHODS: Undergraduate students of year 2017 who majored in Anesthesiology at the Wannan Medical College (China) were chosen as the study subjects. According to the different teaching methods, the students were divided into two groups: 59 in the traditional teaching group (control group) and 61 in the traditional teaching combined with distant live broadcasting teaching group (observation group). The teaching feedback, students' satisfaction, and the theory and skill scores of the course were compared between the two groups. RESULTS: The teaching feedback in the observation group was better than that in the control group (P<0.05). The students' satisfaction rate with teaching and the theory and skill learning score in the observation group were higher than those of the control group (P<0.05). CONCLUSION: Traditional teaching combined with distant live broadcast teaching has achieved good results in clinical anesthesiology teaching, improved the overall quality of teaching, and has high clinical teaching value.

Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression.

Endotoxin-induced lung injury is one of the major causes of death induced by endotoxemia, however, few effective therapeutic options exist. Hydrogen inhalation has recently been shown to be an effective treatment for inflammatory lung injury, but the underlying mechanism is unknown. In the current study we aim to investigate how hydrogen attenuates endotoxin-induced lung injury and provide reference values for the clinical application of hydrogen. LPS was used to establish an endotoxin-induced lung injury mouse model. The survival rate and pulmonary pathologic changes were evaluated. THP-1 and HUVECC cells were cultured in vitro. The thioredoxin 1 (Trx1) inhibitor was used to evaluate the anti-inflammatory effects of hydrogen. Hydrogen significantly improved the survival rate of mice, reduced pulmonary edema and hemorrhage, infiltration of neutrophils, and IL-6 secretion. Inhalation of hydrogen decreased tissue factor (TF) expression and MMP-9 activity, while Trx1 expression was increased in the lungs and serum of endotoxemia mice. LPS-stimulated THP-1 and HUVEC-C cells in vitro and showed that hydrogen decreases TF expression and MMP-9 activity, which were abolished by the Trx1 inhibitor, PX12. Hydrogen attenuates endotoxin-induced lung injury by decreasing TF expression and MMP-9 activity via activating Trx1. Targeting Trx1 by hydrogen may be a potential treatment for endotoxin-induced lung injury.