1.Clinical Study of Three Trembling Needles for Early Parkinson's Disease
Haiwei JIANG ; Chang GAO ; Mengying CAO ; Yanhong YAN ; Qing HU ; Lintong GE
Shanghai Journal of Acupuncture and Moxibustion 2016;35(3):279-281
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.
2.Causal association of obesity and chronic pain mediated by educational attainment and smoking: a mediation Mendelian randomization study
Yunshu LYU ; Qingxing LU ; Yane LIU ; Mengtong XIE ; Lintong JIANG ; Junnan LI ; Ning WANG ; Xianglong DAI ; Yuqi YANG ; Peiming JIANG ; Qiong YU
The Korean Journal of Pain 2025;38(2):177-186
Background:
Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship.
Methods:
This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders.
Results:
The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively.
Conclusions
The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.
3.Causal association of obesity and chronic pain mediated by educational attainment and smoking: a mediation Mendelian randomization study
Yunshu LYU ; Qingxing LU ; Yane LIU ; Mengtong XIE ; Lintong JIANG ; Junnan LI ; Ning WANG ; Xianglong DAI ; Yuqi YANG ; Peiming JIANG ; Qiong YU
The Korean Journal of Pain 2025;38(2):177-186
Background:
Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship.
Methods:
This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders.
Results:
The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively.
Conclusions
The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.
4.Causal association of obesity and chronic pain mediated by educational attainment and smoking: a mediation Mendelian randomization study
Yunshu LYU ; Qingxing LU ; Yane LIU ; Mengtong XIE ; Lintong JIANG ; Junnan LI ; Ning WANG ; Xianglong DAI ; Yuqi YANG ; Peiming JIANG ; Qiong YU
The Korean Journal of Pain 2025;38(2):177-186
Background:
Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship.
Methods:
This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders.
Results:
The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively.
Conclusions
The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.
5.Causal association of obesity and chronic pain mediated by educational attainment and smoking: a mediation Mendelian randomization study
Yunshu LYU ; Qingxing LU ; Yane LIU ; Mengtong XIE ; Lintong JIANG ; Junnan LI ; Ning WANG ; Xianglong DAI ; Yuqi YANG ; Peiming JIANG ; Qiong YU
The Korean Journal of Pain 2025;38(2):177-186
Background:
Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship.
Methods:
This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders.
Results:
The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively.
Conclusions
The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.
6.Causal association of obesity and chronic pain mediated by educational attainment and smoking: a mediation Mendelian randomization study
Yunshu LYU ; Qingxing LU ; Yane LIU ; Mengtong XIE ; Lintong JIANG ; Junnan LI ; Ning WANG ; Xianglong DAI ; Yuqi YANG ; Peiming JIANG ; Qiong YU
The Korean Journal of Pain 2025;38(2):177-186
Background:
Obesity and chronic pain are related in both directions, according to earlier observational research.This research aimed to analyze the causal association between obesity and chronic pain at the genetic level, as well as to assess whether common factors mediate this relationship.
Methods:
This study used bidirectional two sample Mendelian randomization (MR) technique to analyze the association between obesity and chronic pain. Obesity's summary genome-wide association data were obtained from European ancestry groups, as measured by body mass index (BMI), waist-to-hip ratio, waist circumference (WC), and hip circumference (HC), genome-wide association study data for chronic pain also came from the UK population, including chronic pain at three different sites (back, hip, and headache), chronic widespread pain (CWP), and multisite chronic pain (MCP). Secondly, a two-step MR and multivariate MR investigation was performed to evaluate the mediating effects of several proposed confounders.
Results:
The authors discovered a link between chronic pain and obesity. More specifically, a sensitivity analysis was done to confirm the associations between greater BMI, WC, and HC with an increased risk of CWP and MCP.Importantly, the intermediate MR results suggest that education levels and smoking initiation may mediate the causal relationship between BMI on CWP, with a mediation effect of 23.08% and 15.38%, respectively.
Conclusions
The authors’ findings demonstrate that the importance of education and smoking in understanding chronic pain’s pathogenesis, which is important for the primary prevention and prognosis of chronic pain.
7.lncR-GAS5 upregulates the splicing factor SRSF10 to impair endothelial autophagy, leading to atherogenesis.
Yuhua FAN ; Yue ZHANG ; Hongrui ZHAO ; Wenfeng LIU ; Wanqing XU ; Lintong JIANG ; Ranchen XU ; Yue ZHENG ; Xueqing TANG ; Xiaohan LI ; Limin ZHAO ; Xin LIU ; Yang HONG ; Yuan LIN ; Hui CHEN ; Yong ZHANG
Frontiers of Medicine 2023;17(2):317-329
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
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Atherosclerosis/genetics*
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Autophagy/genetics*
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Cell Cycle Proteins/metabolism*
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Endothelial Cells/metabolism*
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Endothelium/metabolism*
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MicroRNAs/metabolism*
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Repressor Proteins/metabolism*
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RNA Splicing Factors
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Serine-Arginine Splicing Factors/genetics*
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RNA, Long Noncoding/metabolism*