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Background: Nervus intermedius neuralgia (NIN), known as geniculate neuralgia (GN), is an uncommon cranial nerve disease caused by an offending vessel compressing the nervus intermedius (NI). Microvascular decompression (MVD) has now become a valued treatment approach for NIN because it can resolve neurovascular conflict (NVC) at the root entry zone of the NI. In the era of continuously optimizing and improving the surgical technique of MVD, further minimization of all possible postoperative complications is not only welcome but also necessary.Objective: The aim of this work is to assess the postoperative outcome of direct visualization of the NI during the MVD procedure.Methods: This study retrospectively reviewed the clinical records of a group of seven consecutive patients with NIN who underwent MVD in the period of 2013–2020 in our clinic and 16 studies reported NIN patients who underwent MVD in the period of 2007–2020.Results: In total, 91.3% of all patients experienced immediate and complete relief of cranial neuralgia after MVD. Six of 23 patients have experienced direct visualization of the NI intraoperatively, and 66.7% of those patients had complications such as facial paralysis, dysacousia, or a combination of these conditions postoperatively. Slight surgical approach-related complications such as complaints associated with excessive drainage of cerebrospinal fluid (CSF), nausea and vertigo, and delayed wound union were observed in 80% of the remaining 15 patients, and these symptoms are totally relieved in the telephone and outpatient follow-up after 6 months.Conclusion: Our case series shows that MVD produced immediate pain relief in the majority of NIN patients. MVD carries surgical risk, especially in patients who experience direct visualization of the NI after mechanical stretch and blunt dissection in surgical procedures. Attempts to avoid mechanical stretch and blunt dissection of the compressed nerve were important for intraoperative neuroprotection, especially facial nerve protection

Traumatic brain injury (TBI) is a major cause of morbidity and mortality, both in adult and pediatric populations. However, the dynamic changes of gene expression profiles following TBI have not been fully understood. In this study, we identified the differentially expressed genes (DEGs) following TBI. Remarkably, Serpina3n, Asf1b, Folr1, LOC100366216, Clec12a, Olr1, Timp1, Hspb1, Lcn2, and Spp1 were identified as the top 10 with the highest statistical significance. The weighted gene coexpression analysis (WGCNA) identified 12 functional modules from the DEGs, which showed specific expression patterns over time and were characterized by enrichment analysis. Specifically, the black and turquoise modules were mainly involved in energy metabolism and protein translation. The green yellow and yellow modules including Hmox1, Mif, Anxa2, Timp1, Gfap, Cd9, Gja1, Pdpn, and Gpx1 were related to response to wounding, indicating that expression of these genes such as Hmox1, Anxa2, and Timp1 could protect the brains from brain injury. The green yellow module highlighted genes involved in microglial cell activation such as Tyrobp, Cx3cr1, Grn, Trem2, C1qa, and Aif1, suggesting that these genes were responsible for the inflammatory response caused by TBI. The upregulation of these genes has been validated in an independent dataset. These results indicated that the key genes in microglia cell activation may serve as a promising therapeutic target for TBI. In summary, the present study provided a full view of the dynamic gene expression changes following TBI.

OBJECTIVE Cushing disease (CD) is a rare clinical disease in which brain structural and function are impaired as the result of excessive cortisol. However, little is known whether rich-club organization changes in patients with CD, as visualized on resting-state magnetic resonance imaging (fMRI), can reverse to normal conditions after transsphenoidal surgery (TSS). In this study, we aimed to investigate whether the functional connectivity of rich-club organization is affected and whether any abnormal changes may reverse after TSS. METHODS In this study, 38 patients with active CD, 33 with patients with CD in remission, and 41 age-, sex-, and education-matched healthy control participants underwent resting-state fMRI. Brain functional connectivity was constructed based on fMRI and rich club was calculated with graph theory approach. We constructed the functional brain networks for all participants and calculated rich-club connectivity based on fMRI. RESULTS We identified left precuneus, right precuneus, left middle cingulum, right middle cingulum, right inferior temporal, right middle temporal, right lingual, right postcentral, right middle occipital, and right precentral regions as rich club nodes. Compared with healthy control participants, rich-club connectivity was significantly lower in patients with active CD (P < 0.001). Moreover, abnormal rich-club connectivity improved to normal after TSS. CONCLUSIONS Our results show rich-club organization was disrupted in patients with active CD with excessive cortisol production. TSS can reverse abnormal rich-club connectivity. Rich club may be a new indicator to investigate the outcomes of TSS and to increase our understanding of the effect of excessive cortisol on brain functional connectivity in patients with CD.

Plasma membrane NADPH oxidases (NOXs), also named respiratory burst oxidase homologues (Rbohs), are critical generators of reactive oxygen species (ROS), which as signal molecules regulate growth and development, and adaptation to various biotic and abiotic stresses in plants. NOXs-dependent ROS production is frequently induced by diverse phytohormones. The ROS commonly function downstream of, and interplay with hormone signalings, coordinately modulating plant development and stress tolerance. In this review, we summarize recent advances on the roles and molecular mechanisms of Rbohs in mediating signalings of multiple hormones including auxin, gibberellins, abscisic acid, ethylene and brassinosteroids in plants.