Three-dimensional (3D) printed models represent educational tools of high quality compared with traditional teaching aids. Colored skull models were produced by 3D printing technology. A randomized controlled trial (RCT) was conducted to compare the learning efficiency of 3D printed skulls with that of cadaveric skulls and atlas. Seventy-nine medical students, who never studied anatomy, were randomized into three groups by drawing lots, using 3D printed skulls, cadaveric skulls, and atlas, respectively, to study the anatomical structures in skull through an introductory lecture and small group discussions. All students completed identical tests, which composed of a theory test and a lab test, before and after a lecture. Pre-test scores showed no differences between the three groups. In post-test, the 3D group was better than the other two groups in total score (cadaver: 29.5 [IQR: 25–33], 3D: 31.5 [IQR: 29–36], atlas: 27.75 [IQR: 24.125–32]; p = 0.044) and scores of lab test (cadaver: 14 [IQR: 10.5–18], 3D: 16.5 [IQR: 14.375–21.625], atlas: 14.5 [IQR: 10–18.125]; p = 0.049). Scores involving theory test, however, showed no difference between the three groups. In this RCT, an inexpensive, precise and rapidly-produced skull model had advantages in assisting anatomy study, especially in structure recognition, compared with traditional education materials.
Epigenetic silencing through methyl-CpG (mCpG) is implicated in many biological patterns such as genome imprinting, X chromosome inactivation, and cancer development. In this process, the mCpG binding domain (MBD) proteins play an essential role in transmitting epigenetic information to downstream regulatory proteins. Among the five MBD proteins identified so far, MBD4 has been the only exception; it has long been thought to be a DNA repair protein. Herein we demonstrate that MBD4 has the ability to repress transcription through mCpG. Transcriptional repression by the MBD4 is histone deacetylase (HDAC) dependent, and MBD4 directly binds to Sin3A and HDAC1 at three central regions that overlap transcriptional repression domains. Furthermore, a chromatin immunoprecipitation assay clearly shows that MBD4 binds to hypermethylated promoters of the p16INK4a and hMLH1 genes. These results suggest that MBD4 is one of the essential components involved in epigenetic silencing in cancer and its repair activity is necessary for the maintenance of hypermethylated promoters.
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