Objective To observe the clinical efficacy of needling the three trembling points plus rehabilitation and taking levodopaand benserazide hydrochlo-ride.Method Ninety-three patients with early Parkinson's disease were randomized into group A of 32 cases, group B of 30 cases, and group C of 31 cases. Group A was intervened by needling the three trembling points plus rehabilitation and taking levodopaand benserazide hydrochlo-ride, group B by rehabilitation and taking levodopaand benserazide hydrochlo-ride, while group C by taking levodopaand benserazide hydrochlo-ride. UPDRSⅢ scores and Berg balance scale (BBS) scores were observed.Result After intervention, UPDRSⅢ scores and BBS scores were significantly changed in all groups (P<0.05). UPDRSⅢ scores of group A were markedly different form that of group B and C (P<0.05). BBS scores of group A and B were markedly different form that of group C (P<0.05).Conclusion Needling the three trembling points plus rehabilitation and taking levodopaand benserazide hydrochlo-ride can improve motor function and equilibrium function in the early Parkinson's disease patients.

Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.
Humans ; Atherosclerosis/genetics* ; Autophagy/genetics* ; Cell Cycle Proteins/metabolism* ; Endothelial Cells/metabolism* ; Endothelium/metabolism* ; MicroRNAs/metabolism* ; Repressor Proteins/metabolism* ; RNA Splicing Factors ; Serine-Arginine Splicing Factors/genetics* ; RNA, Long Noncoding/metabolism*