Case report of CT-guided lung biopsy complicated by air embolism.

Rationale: Cerebral arterial air embolism is a rare but potentially fatal complication of computed tomography (CT) guided lung biopsy. Hyperbaric oxygen (HBO2) is the first line of treatment for arterial gas embolism and needs to be administered immediately after the event. Early HBO2 can reduce the mortality rate of cerebrovascular air embolism. Patient Concerns: A 65-year-old woman was diagnosed with a pulmonary nodule with a diameter of approximately 0.8 cm in the right lower lung. The patient developed consciousness, convulsions, and arrhythmia after CT-guided lung biopsy. Diagnosis: Cranial CT revealed arborizing/linearly distributed gas in the right temporal, parietal, and occipital lobes and left frontal and parietal lobes. Chest CT showed a small amount of pneumothorax. Interventions: The patient was administered HBO2 twice and received other medical treatments and bone flap decompressive craniectomy. Outcomes: The patient developed multiple acute cerebral infarctions and even brain herniation complicated with acute myocardial infarction. Three months after the event, the patient's consciousness was still "open eyes coma" and GCS score was 8t points (E4VtM4). Head CT showed multiple cerebral infarctions and softening lesions. ECG showed sinus rhythm, normal range of the electrocardiogram axis, T wave change, and low voltage on the limb leads. Lessons: Cerebral arterial air embolism is a serious complication of CT-guided lung biopsy. The recommended standard HBO2 should be used as early as possible. However, too severe an injury caused by severe arterial air embolism may not be significantly improved by one to two sessions of HBO2.

A Disintegrin and Metalloproteinase 10 (ADAM10) Is Essential for Oligodendrocyte Precursor Development and Myelination in the Mouse Brain.

A disintegrin and metalloproteinase 10 (ADAM10) plays an essential role in the regulation of survival, proliferation, migration, and differentiation of various neural cells. Nevertheless, the role of ADAM10 in oligodendrocyte precursors (OPCs) and myelination in the central nervous system (CNS) of developing and adult mouse brains is still unknown. We generated ADAM10 conditional knockout (ADAM10 cKO) mice lacking the ADAM10 gene primarily in OPCs by crossing NG2-Cre mice with ADAM10 loxp/loxp mice. We found that OPCs expressed ADAM10 in the mouse corpus callosum and the hippocampus. ADAM10 cKO mice showed significant loss of back hair and reduction in weight and length on postnatal (30 ± 2.1) day, died at (65 ± 5) days after birth, and exhibited the "anxiety and depression-like" performances. Conditional knockout of ADAM10 in OPCs resulted in a prominent increase in myelination and a decrease in the number of OPCs in the corpus callosum at P30 owing to premyelination and lack of proliferation of OPCs. Moreover, the number of proliferating OPCs and mature oligodendrocytes (OLs) also decreased with age in the corpus callosum of ADAM10 cKO mice from P30 to P60. Western blot and RT-PCR results showed that the activation of Notch-1 and its four target genes, Hes1, Hes5, Hey1, and Hey2, was inhibited in the corpus callosum tissue of ADAM10 knockout mice. In our study, we provided experimental evidence to demonstrate that ADAM10 is essential for modulating CNS myelination and OPC development by activating Notch-1 signaling in the developing and adult mouse brain.

Effect of Hyperbaric oxygen on myelin injury and repair after hypoxic-ischemic brain damage in adult rat.

INTRODUCTION: Hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of death and neurological disability with limited options for treatment in neonates, children and adults worldwide. The pathogenesis and treatment of white matter (WM) injury in adult patients with HIE remains largely elusive. METHODS: Sixty male Sprague-Dawley rats were randomly divided into control group, sham-operated group (HBO treatment 6 days after sham operation), and Hypoxia-ischemia (HI) induced brain damage group (receiving left carotid arteries ligation + hypoxia treatment), 1.5ATA hyperbaric oxygen group (HI + 1.5ATA HBOT) and 2.5ATA HBOT group (HI + 2.5ATA HBOT). All the rats were evaluated by water maze before operation, and 6 days after operation, and the function of learning and memory was evaluated; Demyelination in the hippocampus and prefrontal cortex was observed by Luxol fast blue staining (LFB) and MBP immunostaining; the number of Myelin Oligodendrocyte Glycoprotein (MOG),glial fibrillary acidic protein (GFAP), ionic calcium-binding adaptor (Iba-1) and NG2 positive cells in the hippocampus and prefrontal cortex were determined by immunofluorescence staining. The expression of interleukin-1ß (IL-1ß), IL-6 and tumor necrosis factor (TNF-α), Hypoxia Inducible Factor 1 Subunit Alpha (HIF1-α) and Superoxide dismutase (SOD) in brain and serum of rats were measured by Western Blot method and Enzyme linked immunosorbent assay (ELISA). RESULTS: Compared with those in the normal control group and sham-operated group, in the HI group, the learning and memory abilities of rats were significantly decreased (P < 0.05), the intensity of LFB and MBP immunostaining in hippocampus and prefrontal cortex was significantly decreased (P < 0.05); the number of MOG positive oligodendrocytes (OLs) significantly decreased (P < 0.05), whereas the number of Iba-1, GFAP, NG2 positive microglias, astrocytes and oligodendrocyte precursors (OPCs) was increased (P < 0.05); the level of IL-1ß, IL-6, TNF-α and HIF-1a in brain and serum were significantly increased (P < 0.05), whereas SOD was significantly decreased in brain and increased in serum. Compared with those in the HI group, in both 1.5ATA and 2.5ATA HBOT group, the learning and memory abilities were significantly increased (P < 0.05); the intensity of LFB and MBP immunostaining in the hippocampus and prefrontal cortex was significantly increased (P < 0.05); the number of MOG positive OLs significantly increased (P < 0.05); the number of Iba-1, GFAP, NG2 positive microglias, astrocytes and OPCs was decreased (P < 0.05); the level of IL-1ß, IL-6, TNF-α and HIF-1a in brain and serum were significantly decreased (P < 0.05); the level of SOD was significantly increased in brain and decreased in serum. Morever, compared with those in the 1.5ATA group, 2.5ATA provided better treatment results (P < 0.05). CONCLUSION: In the present study, we demonstrated the mechanism of different pressure HBOT on HI induced brain injury from three levels: (1) On a tissue level, HBOT protects against HI induced myelin injury; (2) On a cellular level, HBOT attenuates HI-induced OL loss, suppresss the reactive activation of astrocyte and microglia, and may promote OPC to differentiate into OL; (3) On a molecular level, HBOT inhibites neuroinflammation, and balances oxidative damage and antioxidant capacity. Among the above effects, 2.5ATA HBOT is better than 1.5ATA HBOT. Ongoing research will continue to seek out the signalling pathways and molecules mechanisms on different pressure of HBOT-related myelin protection, and possibly expand suitable HBOT use in adult HIE clinically.