The high level of resistance of glioblastoma multiforme (GBM) to currently used chemotherapies and other conventional therapies, its invasive characteristics and the presence of stem-like cells are the major factors that make the treatment of GBM difficult. Recent studies have demonstrated that the homeostasis of energy metabolism, glycolysis and mitochondrial oxidation of glucose are important for GBM cell growth and chemo-resistance. However, it is not clear which specific gene(s) are involved in the homeostasis of energy metabolism and invasiveness of GBM cells. We performed a preliminary analysis of data obtained from Gene Expression Omnibus profiles and determined that malic enzyme 2 (ME2) expression was positively associated with WHO grade in human primary gliomas. Hence, we evaluated the detailed working mechanisms of ME2 in human GBM cell processes, including proliferation, cell cycle, invasion, migration, ROS, and ATP production. Our data demonstrated that ME2 was involved in GBM growth, invasion and migration. ME2 has two cofactors, NAD+ or NADP+, which are used to produce NADH and NADPH for ATP production and ROS clearance, respectively. If the catalytic activity of ME2 is determined to be critical for its roles in GBM growth, invasion and migration, small molecule inhibitors of ME2 may be valuable drugs for GBM therapy. We hope that our current data provides a candidate treatment strategy for GBM.

Background: The Trachway Videolight Intubating Stylet is a video-assisted system with a rigid but malleable intubating stylet that facilitates endotracheal intubation. Minimizing cervical spine movement with manual in-line stabilization is essential for patients with cervical spine injuries such as multiple trauma. However, the intubation time of the Trachway Videolight Intubating Stylet and complications associated with intubation in patients with manual in-line stabilization in the neutral-head and head-lift positions remain unclear. Methods: Patients (20–80 years old) who were scheduled to undergo surgery that required general anesthesia with tracheal intubation were randomly allocated to either a neutral-head (n = 62) or a head-lift position (n = 62) group. Manual in-line stabilization was performed to limit cervical spine mobility. We aimed to evaluate orotracheal intubation time and success rate in these 2 positions with the Trachway Videolight Intubating Stylet. Results: Intubation was faster in the head-lift than in the neutral-head position (20 ± 10 and 25 ± 13 seconds, respectively, P = .000); intubation was equally successful in the 2 positions (96.8% vs 96.8%). Responses to intubation did not differ between positions (heart rate, P = .142; visual analog scale scores for throat soreness, P = .54). The only significant predictor of intubation time was the body mass index in the head-lift position group (P = .005). Conclusions: Intubation using the Trachway Videolight Intubating Stylet with manual in-line stabilization is faster in the head-lift position, and therefore preferable. However, if the head-lift position is not suitable, the neutral-head position is a sensible alternative, with comparable intubation success rate, heart rate change, and postoperative throat soreness.

In this study, we use animal models combined with bioinformatics strategies to investigate the potential changes in overall renal transcriptional expression after traumatic brain injury. Methods: Microarray analysis was performed after kidney acquisition using unilateral controlled cortical impact as the primary mouse TBI model. Multi-oriented gene set enrichment analysis was performed for differentially expressed genes. Results:The results showed that TBI affected the gene set associated with mitochondria function in kidney cells, and a negative enrichment of gene sets associated with immune cell migration and epidermal development was also observed. Analysis of the disease phenotype gene set revealed that differential expression of mitochondria-related genes was associated with lactate metabolism. Alternatively, activation and adhesion of immune cells associated with the complement system may promote autoinflammation in kidney tissue. The simulated immune cell infiltration analysis showed an increase in the proportion of activated memory CD4 T cells and a decrease in the proportion of resting memory CD4 T cells, suggesting that activated memory CD4 T cell infiltration may be involved in the inflammation of renal tissue and cause damage to renal cells, such as principal cells, mesangial cells and loops of Henle cells. Conclusion:This study is the first to reveal the effects of brain trauma on the kidney. TBI may affect the expression of mitochondria function-related gene sets in renal cells by increasing lactate. It may also affect renal mesangial cells by inducing increased infiltration of immune cells through mechanisms related to complement system activation or autoimmune antibodies.