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Objective: Epistaxis after radiotherapy for nasopharyngeal carcinoma (NPC) is a common clinical critical illness, which often leads to death of patients. This article focuses on the relationship between massive epistaxis and pseudoaneurysm after radiotherapy in patients with NPC and discusses clinically relevant treatment strategies. Methods: A review was performed in 21 patients with massive epistaxis after radiotherapy for NPC from January 2011 to December 2019, and all of the patients were examined by computed tomography angiography (CTA). We also reviewed the English literature over the past 10 years to analyze the characteristics and related causes of pseudoaneurysms in terms of the clinical stage of NPC, course of radiotherapy, and affected artery. An analysis was performed on the methods of endovascular interventional treatment of such pseudoaneurysms. Results: Among the 21 patients, 19 cases had bone destruction of the skull base; 13 cases were also found to have tumor recurrence; 15 cases were in stage III or IV of NPC; pseudoaneurysms were observed in 14 cases, of which nine cases had pseudoaneurysms in the internal carotid artery (ICA), and the rest had pseudoaneurysms in the external carotid artery (ECA). These data were consistent with the results of the literature review. Analysis with imaging revealed that the petrous ICA was the common predilection site. There were 11 out of 14 cases of pseudoaneurysms with sentinel hemorrhage in the initial phase. All 14 pseudoaneurysm patients underwent endovascular interventional therapy, but one died from hemorrhagic shock during the procedure. No rebleeding was observed among the other patients during 72 h after intravascular treatment. Nevertheless, regrettably two patients died on the 10th and 17th days after intervention. Conclusion: Pseudoaneurysm, which was a serious complication after radiotherapy in patients with NPC, could cause massive epistaxis with high mortality. The formation of a pseudoaneurysm was closely associated with a high carcinoma stage, re-radiotherapy, and local bone destruction and infection. Most cases had sentinel epistaxis, which was considered the bleeding characteristic. The imaging material prompted that pseudoaneurysm had a predisposition to the petrous part of the ICA, while the preferred therapy was endovascular embolization treatment. [ABSTRACT FROM AUTHOR]

Neonatal hypoxic-ischemic encephalopathy (HIE) is an obstinate disease that troubles neonatologists. At present, cognitive impairment after HIE has received increasing attention. Synaptic plasticity determines the development of cognitive function, so it is urgent to develop new drugs that can improve HIE-induced cognitive impairment. Hypoxia–ischemia (HI)–induced neuroinflammation affects synaptic plasticity. As a SIRT1 agonist, resveratrol has a powerful anti-inflammatory effect, but whether it has an effect on impaired synaptic plasticity in HIE and the potential mechanism remain unclear. In the present study, resveratrol was used to intervene in hypoxic-ischemic brain injury (HIBI) mice, and the effects on hippocampal synaptic plasticity and further mechanisms were explored through performing neurobehavioral, morphological observations, Golgi sliver staining, western blotting, and quantitative real-time polymerase chain reaction experiments. We first found that resveratrol improves HI-induced long-term cognitive and memory deficits, and then we found that resveratrol reduces hippocampal neuronal damage and increases dendritic spine density and the expression of synaptic proteins. Finally, we found that this effect may be exerted by regulating the neuroinflammatory response mediated by the SIRT1/NF-κB axis. This study provides a new theoretical basis for resveratrol to prevent long-term neurological dysfunction following HIBI. [ABSTRACT FROM AUTHOR]

Th2 cytokines play a pivotal role in the pathogenesis of allergic rhinitis. To investigate the effect of p38 mitogen-activated protein kinase (MAPK) on the production of Th2 cytokines such as IL-4 and IL-5 in allergic rhinitis, a model of allergic rhinitis was established in SD rats. The expression level of p38 MAPK mRNA in PBMCs was detected by means of real time quantitative RT-PCR. The p38 MAPK activity in PBMCs was detected by Western blotting. PBMCs were cultured with various concentrations of p38 MAPK inhibitor SB 239063 or without the treatment, and then IL-4, IL-5 levels of the supernatant were determined by using sandwich ELISA. The results showed that mRNA expression and activity of p38 MAPK in PBMCs were significantly higher in allergic rhinitis rats than in control rats ( P<0.05). The p38 MAPK inhibitor SB 239063 decreased the production of IL-4 and IL-5 in a dose-dependent manner. It is concluded that p38 MAPK plays an important role in the pathogenesis of allergic rhinitis which is associated with Th2 cytokines release. [ABSTRACT FROM AUTHOR]