Qualification of Pilots with Aero-Otitis Media After Balloon Eustachian Tuboplasty.

BACKGROUND: Aero-otitis media (AOM), also known as aural barotrauma or barotitis media, is categorized into primary AOM and secondary AOM. Because conservative treatment was ineffective, primary AOM was one of the main reasons for grounding. In 2014, the team successfully treated a pilot with primary AOM using balloon Eustachian tuboplasty (BET). Now, this case is reported.CASE REPORT:The patient was a 40-yr-old male transport pilot who joined a flight after catching a cold. During the descent, the right ear appeared to have stuffiness and hearing loss, accompanied by tinnitus and ear pain. The local hospital's acoustic immittance test showed an "A" curve in the left ear and a "B" curve in the right ear. According to "secretory otitis media", right tympanic membrane puncture and drugs were performed. After he recovered, he continued to fly, and the symptoms reappeared again. Then he was transferred to our hospital, and right BET was performed. Equalization of ear pressure in the hypobaric chamber returned to normal 2 mo after the operation. The pilot was found fit to fly. The pilot is still qualified, with more than 6000 h of flight time.DISCUSSION: AOM is linked to Eustachian tube dysfunction. BET has been a minimally invasive treatment of Eustachian tube lesions in recent years. If conservative treatments for primary AOM are ineffective, BET can be selected. While the postoperative symptoms disappeared, pure tone audiometry, tympanometry, and ear pressure function tests met the standards for the physical examination of pilots, allowing the determination of flight qualification.Zhang M, Liu X, Wang B, Jin Z, Xu X. Qualification of pilots with aero-otitis media after balloon Eustachian tuboplasty. Aerosp Med Hum Perform. 2023; 94(8):629-633.

Pilots' Spatial Visualization Ability Assessment Based on Virtual Reality.

BACKGROUND: The aim of this study was to investigate the effectiveness of the mental rotation test (MRT) based on virtual reality (VR) in predicting pilots' spatial visualization ability (SVA).METHODS: Based on VR, 118 healthy pilots' SVA were evaluated by MRT. The pilot flight ability evaluation scale was used as the criterion of test validity. According to the scale score, pilots were divided into high, middle, or low spatial ability groups pursuant to the 27% allocation principle. Differences in reaction time (RT), correct rate (CR), and correct number per second (CNPS) of MRT between groups were compared. Correlations between scale scores and MRT scores were analyzed. RT, CR, and CNPS of MRT among different age groups and between genders were also compared.RESULTS: The RT of the high spatial ability group was remarkably slower than that of the low spatial ability group (363.4 ± 140.2 s, 458.1 ± 151.7 s). The CNPS of the high spatial ability group was dramatically higher than that of the low spatial ability group (0.111 ± 0.045 s, 0.086 ± 0.001 s). There were no significant differences in RT, CR, and CNPS between different genders. Pilots in the 29-35 yr old age group had considerably slower RT than those in the 22-28 yr old age group (330.8 ± 140.3 s, 417.2 ± 132.7 s). Pilots in the 29-35 yr old age group had conspicuously higher CNPS than pilots in the 22-28 yr old age group (0.119 ± 0.040 s, 0.096 ± 0.036 s). All pilots' scale scores were positively correlated with CNPS (r = 0.254) and negatively correlated with RT (r = -0.234).DISCUSSION: MRT based on VR has a good discrimination efficacy for SVA of pilots and is a good indicator for the SVA component measurement.Zhang M, Wang M, Feng H, Liu X, Zhai L, Xu X, Jin Z. Pilots' spatial visualization ability assessment based on virtual reality. Aerosp Med Hum Perform. 2023; 94(6):422-428.

[Recombinant adiponectin inhibits the expression of inflammation-associated proteins from mouse astrocytes via AMPK-independent PKC pathway].

Objective To investigate whether recombinant adiponectin peptide (APN) plays an anti-inflammatory role in the oxy-glucose deprivation/reoxygenation (OGD/R) model of astrocytes via the protein kinase C (PKC) and AMP dependent protein kinase (AMPK) pathway. Methods The phosphorylation levels of PKC and AMPK in astrocytic cell line MA1800 was assessed by Western blotting under the condition of OGD/R with the time gradient (2, 4, 6, 8, 12, 24 hours) or the condition of cobalt chloride (CoCl2) treatment with the concentration gradient (20, 50, 100, 200, 400, 600, 800, 1000, 1200, 1600, 2000 µmol/L) to determine the optimal condition of OGD/R in the following study. The cells were grouped into a normal control group, OGD/R treatment group, APN only group, OGD/R combined with APN treatment group, and AMPK inhibition combined with OGD/R and APN treatment group. Western blotting was used to detect the levels of PKCα, phospho-PKC(pan), AMPKα, phospho-AMPKα, NLRP3 inflammasome in the cells, and tumor necrosis factor α (TNF-α) in the conditioned medium of cell culture. Results After OGD/R or 400 µmol/L CoCl2 treatment for 6 hours, the phosphorylation level of p-PKC reached a peak. Compared with the control group, the levels of PKCα, p-AMPKα, AMPK, NLRP3 and TNF-α in the supernatant increased significantly in the experimental groups. Compared with the ODG/R group, the phosphorylation level of PKC, the expression of TNF-α and NLRP3 significantly decreased in the APN treated groups, while the phosphorylation of AMPK remained unchanged. Conclusion APN treatment can inhibit the expression of inflammatory factors in astrocyte model of OGD/R via AMPK-independent PKC signaling pathway.

Comparison of endoscopic evacuation, stereotactic aspiration, and craniotomy for treatment of basal ganglia hemorrhage.

BACKGROUND: The main surgical techniques for spontaneous basal ganglia hemorrhage include stereotactic aspiration, endoscopic aspiration, and craniotomy. However, credible evidence is still needed to validate the effect of these techniques. OBJECTIVE: To explore the long-term outcomes of the three surgical techniques in the treatment of spontaneous basal ganglia hemorrhage. METHODS: Five hundred and sixteen patients with spontaneous basal ganglia hemorrhage who received stereotactic aspiration, endoscopic aspiration, or craniotomy were reviewed retrospectively. Six-month mortality and the modified Rankin Scale score were the primary and secondary outcomes, respectively. A multivariate logistic regression model was used to assess the effects of different surgical techniques on patient outcomes. RESULTS: For the entire cohort, the 6-month mortality in the endoscopic aspiration group was significantly lower than that in the stereotactic aspiration group (odds ratio (OR) 4.280, 95% CI 2.186 to 8.380); the 6-month mortality in the endoscopic aspiration group was lower than that in the craniotomy group, but the difference was not significant (OR=1.930, 95% CI 0.835 to 4.465). A further subgroup analysis was stratified by hematoma volume. The mortality in the endoscopic aspiration group was significantly lower than in the stereotactic aspiration group in the medium (≥40-<80 mL) (OR=2.438, 95% CI 1.101 to 5.402) and large hematoma subgroup (≥80 mL) (OR=66.532, 95% CI 6.345 to 697.675). Compared with the endoscopic aspiration group, a trend towards increased mortality was observed in the large hematoma subgroup of the craniotomy group (OR=8.721, 95% CI 0.933 to 81.551). CONCLUSION: Endoscopic aspiration can decrease the 6-month mortality of spontaneous basal ganglia hemorrhage, especially in patients with a hematoma volume ≥40 mL.

Pterostilbene Attenuates Astrocytic Inflammation and Neuronal Oxidative Injury After Ischemia-Reperfusion by Inhibiting NF-κB Phosphorylation.

Astrocyte-mediated inflammation and oxidative stress elicit cerebral ischemia-reperfusion (IR) injury after stroke. Nuclear factor (NF)-κB activates astrocytes and generates pro-inflammatory factors. The purpose of the present study is to elucidate the effect of pterostilbene (PTE, a natural stilbene) on astrocytic inflammation and neuronal oxidative injury following cerebral ischemia-reperfusion injury. A middle cerebral artery occlusion-reperfusion (MCAO/R) mouse model and HT22/U251 co-culture model subjected to oxygen-glucose deprivation and re-introduction (OGD/R) were employed, with or without PTE treatment. The data showed that PTE delivery immediately after reperfusion, at 1 h after occlusion, decreased infarct volume, brain edema, and neuronal apoptosis and improved long-term neurological function. PTE decreased oxidation (i.e., production of reactive oxygen species, malondialdehyde) and inflammatory mediators (tumor necrosis factor-α, interleukin-1ß, and interleukin-6) and increased anti-oxidative enzyme activities (i.e., of superoxide dismutase, glutathione peroxidase), by inhibiting phosphorylation and nuclear translocation of NF-κB. In conclusion, PTE attenuated astrocyte-mediated inflammation and oxidative injury following IR via NF-κB inhibition. Overall, PTE is a promising neuroprotective agent.

Adiponectin confers neuroprotection against cerebral ischemia-reperfusion injury through activating the cAMP/PKA-CREB-BDNF signaling.

Ischemic stroke is a severe cerebrovascular disease. Although great progress has been made, the consequent ischemia-reperfusion (I/R) injury is inevitable and affects the therapeutic effect. Adiponectin (APN) is a fat-derived plasma protein that has beneficial actions on cardiovascular disorders. The present study aims to investigate the effect of APN on I/R injury and the potential underlying mechanisms. In step 1, APN were administered for three times (once every 8 h) 24 h before middle cerebral artery occlusion (MCAO). The results indicated that APN treatment reduced infarct volume, neurological deficits and brain water content after I/R injury. Meanwhile, APN was proved to increase the expression of cAMP, PKA, CREB, and BDNF. In step 2, mice were randomly assigned into the Vehicle + I/R, APN + I/R, PKA activator + I/R, PKA inhibitor + APN + I/R groups. PKA activator, PKA inhibitor, as well as APN were administered for three times before MCAO. The results indicated that PKA inhibitor downregulated the expressions of cAMP, PKA, CREB, and BDNF which subsequently weakened the protective effects of APN on cerebral I/R injury. In conclusion, our findings further suggest that APN exerts protective effect against cerebral I/R injury might through the cAMP/PKA-CREB-BDNF signaling pathway. APN is a novel candidate in the treatment of I/R diseases in the future.

Adiponectin Attenuates Oxygen-Glucose Deprivation-Induced Mitochondrial Oxidative Injury and Apoptosis in Hippocampal HT22 Cells via the JAK2/STAT3 Pathway.

Ischemic stroke is among the leading causes of morbidity and mortality worldwide. Improving the tolerance of neurons to ischemia and reperfusion injury could be a feasible strategy against ischemia. Adiponectin (APN) is a major adipokine that regulates glucose and lipid metabolism and plays an important role in the protection of the cerebral nervous system. We aimed to investigate the effects of APN on oxygen and glucose deprivation (OGD)-induced neuronal injury in hippocampal neuronal HT22 cells. APN displayed neuroprotective effects against OGD, evidenced by increased cell viability and decreased lactate dehydrogenase release and apoptotic rate. Additionally, APN also maintained mitochondrial ultrastructure and transmembrane potential, attenuated reactive oxygen species and malondialdehyde, and increased superoxide dismutase and glutathione peroxidase activity. Moreover, APN promoted Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) phosphorylation, enhanced STAT3 nuclear translocation, increased the Bcl-2/Bax ratio, and decreased cleaved caspase-3. The aforementioned APN-induced effects were almost reversed by a JAK2 inhibitor, AG490. APN may attenuate OGD-induced hippocampal HT22 neuronal impairment by protecting cells against mitochondrial oxidative stress and apoptosis, mediated by JAK2/STAT3 signaling.

Predominant neuronal differentiation of Olig1+ neural progenitors in forebrain cortex biased by ß-catenin over-expression.

Proper neuron-glia ratio is essential for normal brain development and function. Olig1 is a basic helix-loop-helix (bHLH) transcription factor generally used as a lineage tool for oligodendrocyte research in spinal cord. Recent studies have revealed a property of Olig1-positive cells as the common progenitors of GABAergic neurons and oligodendrocytes in the forebrain during embryogenesis, and a stage-dependent regulatory role of Wnt/ß-catenin signaling in the differentiation of oligodendrocytes in spinal cord. Given the neurogenic role of Wnt/ß-catenin signaling in neural progenitor cells, it is unclear how ß-catenin affects the differentiation of Olig1-positive progenitors in brain. In the present study, we investigated the effects of ß-catenin over-expression on the differentiation of Olig1-positive progenitors in the forebrain cortex, by using Olig1-Cre:ß-cateninEX3 (loxp/+):ROSA-YFP (ß-cateninEX3 CKO) mice as compared to Olig1-Cre:ROSA-YFP control. The results showed that in the cortex of Olig1-Cre:ROSA-YFP mice, approximately 28.6% of YFP labeled cells are GFAP-positive, 43.7% are NG2-positive, 23.4% are CC1-positive and 3.2% are NeuN-positive, showing that Olig1-positive cells are multi-potential and mainly gliogenic. However, in the cortex of ß-cateninEX3 CKO mice, the percentage of astrocytes generated from Olig1-positive cells decreased dramatically to approximately 2%, NG2-positive cells to 0.4%, and CC1-positive cells to 0.5%. In contrast, the percentage of NeuN-positive cells increased to approximately 96% of YFP-labeled cells. Taken together, our data showed that the gliogenic property of Olig1-positive progenitors in forebrain can be efficiently switched to neurogenic by over-expressing ß-catenin, revealing a neurogenic effect of ß-catenin in the forebrain Olig1-positive progenitors.

Wnt/ß-catenin signaling mediates the seizure-facilitating effect of postischemic reactive astrocytes after pentylenetetrazole-kindling.

Ischemia not only leads to tissue damage, but also induces seizures, which in turn worsens the outcome of ischemia. Recent studies have revealed the impaired homeostatic functions of reactive astrocytes, which were thought to facilitate the development of seizures. However, how this phenotype of reactive astrocytes is regulated remains unclear. Here, using pentylenetetrazole (PTZ)-kindling model, we investigated the roles of reactive astrocytes and their intracellular Wnt/ß-catenin signaling in the ischemia-increased seizure susceptibility. Our data showed that somatosensory cortical ischemia significantly increased the susceptibility to PTZ-induced seizure. Genetic ablation of Nestin-positive reactive astrocytes significantly decreased the incidence and severity of seizures. By using a Wnt signaling reporter mice line Topgal mice, we found that Wnt/ß-catenin signaling was upregulated in reactive astrocytes after ischemia. Depletion of ß-catenin in reactive astrocytes significantly decreased the susceptibility of seizures and the expression of c-Fos induced by PTZ in the ischemic cortex. Overexpression of ß-catenin in reactive astrocytes, in contrast, significantly increased seizure susceptibility and the expression of c-Fos. Furthermore, the expression of aquaporin-4 (AQP-4) and inwardly rectifying K(+) channel 4.1 (Kir4.1), two molecules reportedly associated with seizure development, was oppositely affected in reactive astrocytes with ß-catenin depletion or overexpression. Taken together, these data indicated that astrocytic Wnt/ß-catenin signaling accounts, at least partially, for the ischemia-increased seizure susceptibility. Inhibiting Wnt/ß-catenin signaling may be utilized in the future for preventing postischemic seizures.