SGK1 in Schwann cells is a potential molecular switch involved in axonal and glial regeneration during peripheral nerve injury.

Schwann cells play an important role in peripheral myelination, and dysfunction of these cells leads to axonal damage. Schwann cells degenerate following peripheral nerve injury. Immature Schwann cells proliferate, differentiate, and support axonal regeneration and extension during recovery. There are a lot of intracellular signals involved in the myelination process. Although serum- and glucocorticoid-inducible kinase (SGK1) in Schwann cells is supposedly involved in developmental myelination, its significance during peripheral nerve injury and repair remains unknown. In this study, we examined the dynamics of SGK1 during peripheral nerve repair and the potential role of SGK in the process. Axonal crush injury was first generated in the right sciatic nerve under anesthesia in mice, which exhibited apparent paralysis and subsequent recovery of the injured hindlimbs. Immunohistochemical analysis revealed the appearance of glial fibrillary acidic protein (GFAP)-positive immature Schwann cells around injured nerves, and SGK1 was present in these cells. Next, we employed S16 cells, a Schwann cell line, to explore the impact of SGK1 on Schwann cells. Administration of the SGK inhibitor gsk650394 decreased cell proliferation and increased cell size. SGK inhibition did not cause cellular injury, suggesting that it suppresses proliferation and enlarges Schwann cells without causing cell death. Furthermore, quantitative PCR and immunoblotting revealed that SGK inhibition upregulated the gene expression of BDNF, MBP, and Krox20, which are facilitating factors for myelination and neural regeneration, and downregulated that of Sox10. Taken together, these findings indicate that SGK1 inactivation in Schwann cells diverts cell fate from proliferation to differentiation.

Brain abscess of odontogenic origin in patients with malignant tumors: A report of two cases.

BACKGROUND: Oral infection and dental manipulations can lead to the development of brain abscesses, a rare but potentially life-threatening condition. Herein, we report patients undergoing cancer treatment who developed brain abscesses of odontogenic origin at our hospital. CASE DESCRIPTION: Two patients developed brain abscesses during cancer treatment. Both underwent neurosurgical aspiration, and the causative microorganism was identified as Streptococcus intermedius of the Streptococcus anginosus group, which is a part of the normal bacterial flora in the oral cavity. There was clinical and radiographic evidence of dental infection in one of the patients diagnosed with a brain abscess of odontogenic origin. No infectious foci were found in the other patient during hospitalization for the abscess. However, the patient had undergone extraction of an infected tooth approximately 3 months before admission for the abscess, suggesting origination from an oral infection or dental manipulation. The patients' cancers rapidly worsened because cancer treatment in both patients was interrupted for several months to treat the brain abscess. CONCLUSION: Oral infections can cause severe infections, such as brain abscesses, particularly during the treatment of malignant tumors. Improving the oral environment or treating oral infections before initiating treatment for malignant tumors is highly recommended. In addition, the possibility of odontogenic origin should always be considered as a potential etiology of brain abscesses.