investigating-alterations-caecum-microbiota-after-traumatic-brain

Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice

Increasing evidence shows that the microbiota-gut-brain axis plays an important role in the pathogenesis of brain diseases. Several studies also ...

Zhejiang University

Chronic subdural hematoma (CSDH) is a common disease in neurosurgical practice with substantial recurrence rate. We aimed to estimate recurrence rate of CSDH and to identify risk factors for CSDH recurrence.

Prevalence of and risk factors for recurrence of chronic subdural hematoma.

Increasing evidence indicates that activated microglia play an important role in the inflammatory response following traumatic brain injury (TBI). Inhibiting M1 and stimulating M2 activated microglia have demonstrated protective effects in several animal models of central nervous system diseases. However, it is not clear whether the polarization of microglia to M2 attenuates axonal injury following TBI. In this study, we used a lateral fluid percussion injury device to induce axonal injury in mice. Mice were randomly assigned to the sham, TBI, TBI + rosiglitazone (peroxisome proliferator-activated receptor gamma [PPAR-γ] agonist), and TBI + GW9662 (PPAR-γ antagonist) groups. Axonal injury was assessed using immunohistochemical staining for beta amyloid precursor protein. The inflammatory response was assessed by enzyme-linked immunosorbent assay, microglia polarization was assessed using specific markers of M1 and M2 microglia, and neurological function was assessed using the neurological severity score. Following TBI, microglia of the M1 phenotype increased significantly, while those of the M2 phenotype decreased. Rosiglitazone-induced PPAR-γ activation promoted microglia polarization to the M2 phenotype, which reduced the inflammatory response, attenuated axonal injury in the cerebral cortex, and improved neurological function. Conversely, GW9662 inhibited the polarization of microglia to M2 and aggravated inflammation and axonal injury. Our in vitro findings in lipopolysaccharide-induced microglia were consistent with those of our in vivo experiments. In conclusion, the polarization of microglia to the M2 phenotype via PPAR-γ activation attenuated axonal injury following TBI in mice, which may be a potential therapeutic approach for TBI-induced axonal injury.

Polarization of Microglia to the M2 Phenotype in a Peroxisome Proliferator-Activated Receptor Gamma-Dependent Manner Attenuates Axonal Injury Induced by Traumatic Brain Injury in Mice.

Hyperbaric oxygen therapy (HBOT) is an efficient therapeutic option to improve progress of lots of diseases especially hypoxia-related injuries, and has been clinically established as a wide-used therapy for patients with carbon monoxide poisoning, decompression sickness, arterial gas embolism, problematic wound, and so on. In the liver, most studies positively evaluated HBOT as a potential therapeutic option for liver transplantation, acute liver injury, nonalcoholic steatohepatitis, fibrosis and cancer, especially for hepatic artery thrombosis. This might mainly attribute to the anti-oxidation and anti-inflammation of HBOT. However, some controversies are existed, possibly due to hyperbaric oxygen toxicity. This review summarizes the current understandings of the role of HBOT in liver diseases and hepatic regeneration. Future understanding of HBOT in clinical trials and its in-depth mechanisms may contribute to the development of this novel adjuvant strategy for clinical therapy of liver diseases.

Hyperbaric Oxygen Therapy in Liver Diseases.

Cranioplasty is a common procedure in neurosurgical practice. However, some complications may occur after the operation. We here presented a case of bilateral skull defect and underwent cranioplasty with polyetheretherketone (PEEK) prosthesis. The patient developed epidural effusion on both sides 7 days after surgery. The effusion was light yellow and transparent, and laboratory examinations revealed normal glucose level, negative bacteriological results, and increased IgG protein concentration. The effusion disappeared after treatment with dexamethasone and drainage. We speculated that the epidural effusion was because of delayed type allergic reactions after PEEK cranioplasty. However, further studies are needed to investigate its related mechanisms.

Allergic Epidural Effusion Following Polyetheretherketone Cranioplasty.

Hypopituitarism is a common but potentially undiagnosed complication in patients who suffer traumatic brain injury (TBI). The identification of risk factors of hypopituitarism after TBI is vital to establish a rational testing approach for these patients.

Article	Year
Prevalence of and risk factors for recurrence of chronic subdural hematoma. Acta neurochirurgica\| PubMed ID: 29532258	2018
Polarization of Microglia to the M2 Phenotype in a Peroxisome Proliferator-Activated Receptor Gamma-Dependent Manner Attenuates Axonal Injury Induced by Traumatic Brain Injury in Mice. Journal of neurotrauma\| PubMed ID: 29649924	2018
Hyperbaric Oxygen Therapy in Liver Diseases. International journal of medical sciences\| PubMed ID: 30008587	2018
Allergic Epidural Effusion Following Polyetheretherketone Cranioplasty. The Journal of craniofacial surgery\| PubMed ID: 30730518	2019
Risk Factors for Anterior Hypopituitarism in Patients With Traumatic Brain Injury. The Journal of craniofacial surgery\| PubMed ID: 30950947	2019

Wendong You

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