Mucin 1 and poly I:C activates dendritic cells and effectively eradicates pituitary tumors as a prophylactic vaccine.

Pituitary tumors are the most common type of cancer within the central nervous system. In the present study, the expression levels of mucin 1 (Muc1) were examined in invasive and non­invasive pituitary tumor samples, and the results of immunohistochemical staining and Western blot analysis demonstrated marked positive expression of Muc1. In addition, Muc1 + polyinosinic:polycytidylic acid (poly I:C) was found to stimulate the expression levels of the surface molecules cluster of differentiation (CD)40, CD83 and CD80, and HLA­DRm and decreased the expression of CD14 in the dendritic cells, determined using fluorescence­activated cell sorting. The secretions of interleukin (IL)­6, tumor necrosis factor­α and IL­1ß cytokines were also significantly induced, in a dose­dependent manner. In in vivo experiments, a higher percentage of CD3+CD4+ T lymphocytes was detected, and the levels of interferon­Î³ and IL­2 in the splenocytes were also upregulated. Furthermore, the combination treatment of Muc1 with poly I:C increased anti­Muc1 IgM and anti­Muc1 IgG titers, and altered the balance of IgG2a and IgG1, all of which increased the T helper (Th)1 polarized immune response. Thus, the tumor antigen, Muc1, with poly I:C may produce potent protective effects, which polarize immune responses towards Th1, and elicit antitumor immunity to inhibit the progression of pituitary tumors.

Three-dimensional printing models improve understanding of spinal fracture--A randomized controlled study in China.

Three-dimensional printing (3 Dp) is being increasingly used in medical education. Although the use of such lifelike models is beneficial, well-powered, randomized studies supporting this statement are scarce. Two spinal fracture simulation models were generated by 3 Dp. Altogether, 120 medical students (54.2% females) were randomized into three teaching module groups [two-dimensional computed tomography images (CT), 3D, or 3 Dp] and asked to answer 10 key anatomical and 4 evaluative questions. Students in the 3 Dp or 3D group performed significantly better than those in the CT group, although males in the 3D group scored higher than females. Students in the 3 Dp group were the first to answer all questions, and there were no sex-related differences. Pleasure, assistance, effect, and confidence were more predominant in students in the 3 Dp group than in those in the 3D and CT groups. This randomized study revealed that the 3 Dp model markedly improved the identification of complex spinal fracture anatomy by medical students and was equally appreciated and comprehended by both sexes. Therefore, the lifelike fracture model made by 3 Dp technology should be used as a means of premedical education.

17AAG improves histological and functional outcomes in a rat CCI model through autophagy activation and apoptosis attenuation.

Traumatic brain injury (TBI) is caused by both primary and secondary injury mechanisms, all of which cause neuronal cell death and functional deficits. Both apoptosis and autophagy participated in neuronal cell death and functional loss induced following TBI. Preclinical findings implicate that 17-allylamino-demethoxygeldanamycin (17-AAG), an anticancer drug in clinical, present neuroprotection actions in multiple neurological disorders, but whether 17-AAG is capable of modulating neuronal autophagy has never been addressed. The present study was designed to determine the hypothesis that17-AAG treatment could confer neuroprotection in a rat model of TBI. We also used an autophagy inhibitor 3-methyladenine (3-MA) as well as an autophagy inducer rapamycin (RAPA) to test its underlining mechanisms. Our results showed that post-TBI administration of 17-AAG could attenuate brain edema, decrease neuronal death, as well as improve the recovery of motor function. Afterwards, in our model, 17-AAG treatment protected against TBI-induced apoptosis activation as well as enhanced neuronal autophagy. The present study provides novel clues in understanding the mechanisms of which 17-AAG exerts its neuroprotective activity on neurological disorders.