With the further development of endoscopic technology and the application of minimally invasive concept in the diagnosis and treatment of colorectal surgery diseases, the diagnosis and treatment of colorectal related diseases have undergone tremendous changes. Surgical diagnosis and treatment of colorectal diseases have achieved great results in the minimally invasive field, ranging from traditional transabdominal surgery to laparoscopic surgery, transvaginal surgery, and transvaginal specimen removal. One of the most cutting-edge surgical methods in the field of minimally invasive colorectal surgery at present, this method avoids the incision in the abdominal wall by taking specimens through the rectum and vagina, thus further minimally invasive colorectal surgery. The NOSES technology combines the advantages of traditional laparoscopic surgery with the concept of modern minimally invasive surgery. It embodies the characteristics of minimally invasive, fast track rehabilitation in surgery, functional surgery and other concepts on the basis of ensuring the operation effect. This paper mainly summarizes the relevant experience, experience and experience in the development of colorectal surgery diagnosis and treatment by carrying out the nose technology at home and abroad.

Myoclonus dystonia syndrome (MDS) is an inherited movement disorder, and most MDS-related mutations have so far been found in the ε-sarcoglycan (SGCE) coding gene. By generating SGCE-knockout (KO) and human 237 C > T mutation knock-in (KI) mice, we showed here that both KO and KI mice exerted typical movement defects similar to those of MDS patients. SGCE promoted filopodia development in vitro and inhibited excitatory synapse formation both in vivo and in vitro. Loss of function of SGCE leading to excessive excitatory synapses that may ultimately contribute to MDS pathology. Indeed, using a zebrafish MDS model, we found that among 1700 screened chemical compounds, Vigabatrin was the most potent in readily reversing MDS symptoms of mouse disease models. Our study strengthens the notion that mutations of SGCE lead to MDS and most likely, SGCE functions to brake synaptogenesis in the CNS.