Radiotherapy (RT) is the primary treatment for nasopharyngeal carcinoma (NPC). In order to achieve tumor control, nearby normal brain tissues, especially the temporal lobes, often receive unnecessary radiation. Patients with NPC treated by RT may occur cognitive impairments, which significantly compromises the quality of life. The symptoms of cognitive dysfunction induced by RT in NPC patients can exhibit at the early or later stage after RT, which may be related to temporal lobe injury or brain damage induced by radiation. However, the relationship between the cognitive declines induced by RT and the radiation dose or volume of the temporal lobe (or the dosimetry to treat NPC) has not yet been definitively established, and few reports have focused on cognitive impairment following intensity modulated RT. Therefore, this paper will review the progress in radiation-induced cognitive decline of NPC patients in order to provide the basis for preventing side effects of RT and improving the quality of life after RT.

Objective To investigate the effect of different doses of dexmedetomidine (DEX) on myocardial ischemia-reperfusion injury (MIRI) in rats.Methods Seventy-five SD male rats weighing between 250 and 300g were divided into sham group,MIRI group,small-dose DEX group,medium-dose DEX group and high-dose group according to the random number table,with 15 rats per group.Threading the left anterior descending coronary artery was done only in sham group,but the MIRI model was produced in the rest groups by ligation of the artery for 30 minutes followed by 120 minutes of reperfusion.Fifteen minutes before the ligation,small-,medium-and high-dose DEX groups were injected 2.5,5 and 10 μg · kg-1 · h-1 of DEX respectively until the end of reperfusion.Instead,an equal volume of normal saline was given in sham and MIRI groups.At the end of reperfusion,five rats in each group were used to determine the myocardial infarct size,and arterial blood samples and myocardial tissues from ten rats in each group were used to measure serum levels of interleukin-1β (IL-β) and serum tumor necrosis factor-α (TNF-α),expression of myocardial nuclear factor kappa B p65 (NF-κB p65) and change of myocardial pathomorphology.Results Myocardial infract size,degree of myocardial pathomorphology structure damage,serum levels of IL-1 β and TNF-αt and expression of myocardial NF-κB p65 in sham group were significantly lower in sham group than other groups (P ＜ 0.05).Above mentioned parameters in small-,medium-and high-dose DEX groups were all significantly decreased compared to MIRI group (P ＜ 0.05),and the decrease was most significant in medium-dose DEX group (P ＜ 0.05).Conclusions DEX can attenuate the MIRI in rats and the possible mechanism is suppressing the release of NF-κB p65,which can reduce serum pro-inflammatory cytokines like TNF-α and IL-1β.And mediumdose DEX exhibits better protective effect.

Objective To investigate the effect of state anxiety and trait anxiety on attentional orienting of heroin addicts. Methods State anxiety and trait anxiety was measured by State-Trait Anxiety Inventory (STAI). Forty heroin ad?dicts (36 males and 4 females) and 40 healthy controls (36 males and 4 females) participated in cue-target task. Atten?tional orienting and reorienting were measured in valid cue trials and invalid cue trails. Results Heroin addicts had sig?nificantly greater state anxiety [(42.65 ± 6.58) vs. (36.60 ± 8.91)] and trait anxiety [(44.43 ± 7.67) vs. (37.00 ± 8.63)] values than controls (P<0.05). The state anxiety was significantly correlated with orientation RT difference (r=-0.259, P=0.020) and disengaging/reorientation RT difference (r=0.333, P=0.003) in heroin addicts. Trait anxiety was also significantly cor?related with orientation RT difference (r=-0.248, P=0.026) and disengaging/reorientation RT difference (r=0.356, P=0.001) in heroin addicts. Conclusion Heroin addicts have significantly greater anxiety than healthy controls. Both their state anxiety and trait anxiety are associated with attentional orienting and disengaging/reorienting.

Nerve toxicity, such as cognitive dysfunction, often appears in patients with brain tumors after radiotherapy. Cognitive dysfunction after radiotherapy can even appear in patients with extra-cranial tumors such as head and neck cancers. These declines in cognition can seriously affect the patient's quality of life. Therefore, it is very important to find a clear mechanism of brain ionization radiation induced cognitive impairment. At present, the exact mechanism of brain ionization radiation induced cognitive impairment is unclear, and it may be mainly associated with the decline of hippocampal neurogenesis, changes of microenvironment, inflammation, oxidative stress, vascular injury and blood-brain barrier damage, dendritic morphology and N-methyl- D aspartate changes. This review summarizes the recent advance in main mechanism of brain ionization radiation induced cognitive impairment.