1.Analysis and classification of functional dyspepsia
Hong TIAN ; Hanjian ZHOU ; Lan GE
Clinical Medicine of China 2000;0(11):-
Objective To investigate the proportions of the functional dyspepsia (FD) subgroups and to explore theri relationship with Helicobacter pylori (HP).Methods 186 cases with FD received questionaires about their condition and were typed according to their symptom.HP was detected through urease test,spear technique and cultivation.Results The proportion and HP-positive rate of the subgroup were 11.29%,14.24% in reflux-type dyspepsia,13.98%,46.15% in ulcer-type dyspepsin,48.39%,41.11% in dysmotility-type dyspepsia and 26.34%, 38.78% in complex dyspepsia,respectively.The total HP-positive rate of FD is 38.17%.Conclusion Dysmotility-type dyspepsia is most common.Some subgroups are overlapping with each other.There is no relationship between FD and HP.The HP-positive rate of the reflux-type dyspepsia is lower.This observation suggests that HP may have protective effects on esophagus.
2. Mutation in ε-Sarcoglycan Induces a Myoclonus-Dystonia Syndrome-Like Movement Disorder in Mice
Jiao LI ; Yiqiong LIU ; Qin LI ; Xiaolin HUANG ; Dingxi ZHOU ; Hanjian XU ; Feng ZHAO ; Xiaoxiao MI ; Jing YANG ; Dong LIU ; Xuliang DENG ; Yan ZHANG ; Fan JIA ; Fuqiang XU ; Ruoxu WANG
Neuroscience Bulletin 2021;37(3):311-322
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.