BACKGROUND:Electromyographic biofeedback therapy has demonstrated unique advantages of non-invasive,real-time feedback,personalized treatment and promotion of neuroplasticity,and can promote the recovery of motor function in patients with spinal cord injury.OBJECTIVE:To review the current application status and therapeutic effects of electromyographic biofeedback combined with exercise therapy,robotic exoskeletons,and virtual reality technology in the recovery of motor function after spinal cord injury.METHODS:Relevant literature was retrieved from CNKI and PubMed databases up to May 2024.The search terms included"spinal cord injury,EMG biofeedback,physical therapy,robotic exoskeleton,VR,motor function,exercise"in both English and Chinese.Finally,71 articles were included for review.RESULTS AND CONCLUSION:Mechanisms by which electromyographic biofeedback therapy promotes spinal cord injury rehabilitation include promoting neural plasticity changes,strengthening neuromuscular connections and improving movement patterns.Electromyographic biofeedback,as an emerging tool for treating spinal cord injury,is often used in conjunction with other therapeutic methods,including exercise therapy,robotic exoskeletons,and VR,to promote the recovery of motor function after spinal cord injury.The effectiveness of combination therapy has been significantly improved.However,there are still some problems and challenges,such as the lack of detailed analysis of the mechanism,the lack of large-scale trials that provide strong evidence for combined efficacy,and the limited adaptability of the technology.Future research can focus on these aspects:to improve the personalization and accuracy of electromyographic biofeedback;to develop new rehabilitation equipment and expand the application areas of electromyographic biofeedback combined with more advanced technologies or engineering equipment;to apply electromyographic biofeedback to gait training systems,respiratory training systems,and limb-linkage rehabilitation systems,so as to improve the accuracy of the feedback and the effect of personalized treatment plans.At the same time,the ease of use and comfort of the equipment will be improved.

Objective To explore the correlation between serum circularRNA-HOMER1(circHOMER1),microRNA(miR)-23a-3p levels with clinical stages and oxidative stress in patients with diabetic retinopathy(DR).Methods From January 2023 to July 2024,75 DR patients treated in Handan Central Hospital were included as the DR group.According to the clinical staging of DR,they were divided into non proliferative DR(NPDR group,n=43)and proliferative DR(PDR group,n=32).In addition,75 patients with simple type 2 diabetes who came to Handan Central Hospital were included as non DR group.The levels of serum circHOMER1,miR-23a-3p,malondialdehyde(MDA),superoxide dismutase(SOD),and reduced glutathione(GSH)were detect-ed.Clinical data of the subjects were collected.The TargetScan website was used to predict the targeting relationship between circHOMER1 and miR-23a-3p.Pearson method was used to analyze the correlation between serum circHOMER1,miR-23a-3p and MDA,SOD,GSH.Univariate and multivariate Logistic regression were used to analyze the influencing factors of progression of DR in type 2 diabetes patients.Receiver operating characteristic(ROC)carve was used to analyze the predictive value of serum circHOMER1 and miR-23a-3p in the progression of DR in patients with type 2 diabetes.Results There was a targeted relationship between circHOMER1 and miR-23a-3p.The serum MDA(28.66±4.52ng/ml)and circHOMER1(1.24±0.16)levels in the DR group were higher than those in the non DR group(16.95±3.27ng/ml,1.02±0.11),while SOD(45.39±7.84U/L),GSH(135.82±21.23μg/mL)and miR-23a-3p(0.88±0.07)levels were lower than those in the non DR group(81.65±11.47U/L,207.44±25.95μg/mL,1.01±0.09),and differences were statistically significant(t=9.813～22.602,all P<0.001).The serum MDA(33.28±4.96ng/ml)and circHOMER1(1.36±0.20)levels in the PDR group were higher than those in the NPDR group(25.23±3.58ng/ml,1.15±0.17),while SOD(34.39±7.15U/L),GSH(113.50±20.17μg/ml)and miR-23a-3p(0.79±0.07)levels were lower than those in the NPDR group(53.27±8.44U/L,152.43±23.99μg/ml,0.94±0.08),and the differences were statistically significant(t=4.906～10.376,all P<0.001).Spearman analysis showed that serum MDA and circHOMER1 were positively correlated with the severity of DR(r=0.533,0.473,all P<0.001),while SOD,GSH,miR-23a-3p were negatively correlated with the severity of DR(r=-0.552,-0.515,-0.529,all P<0.001).Pearson analysis showed that serum circHOMER1 was negatively correlated with miR-23a-3p,SOD,GSH,and positively correlated with MDA(r=-0.475,-0.460,-0.455,0.462,all P<0.001).Serum miR-23a-3p was positively correlated with SOD and GSH,and negatively correlated with MDA(r=0.428,0.437,-0.439,all P<0.001).Logistic regression analysis showed that high MDA,low SOD,low GSH,high circHOMER1,low miR-23a-3p,high FPG and high HbA1c were the risk factors of progression of DR in type 2 diabetes patients(OR=0.214～3.556,all P<0.05).The area under curve(AUC)of serum circHOMER1 and miR-23a-3p alone and jointhy predicting the progression of DR in type 2 diabetes patients were 0.751,0.797 and 0.903 respectively.The combined prediction was higher than that of serum circHOMER1 and miR-23a-3p alone(Z=3.179,2.335,P=0.002,0.020).Conclusion Serum MDA and circHOMER1 levels are higher in DR patients,while serum SOD,GSH and miR-23a-3p levels are lower.Abnormal expression of circHOMER1 and miR-23a-3p in serum is associated with progression of DR and oxidative stress.Combined detection of circHOMER1 and miR-23a-3p in serum can predict the progression of DR in patients with type 2 diabetes.

Objective To explore the correlation between serum circularRNA-HOMER1(circHOMER1),microRNA(miR)-23a-3p levels with clinical stages and oxidative stress in patients with diabetic retinopathy(DR).Methods From January 2023 to July 2024,75 DR patients treated in Handan Central Hospital were included as the DR group.According to the clinical staging of DR,they were divided into non proliferative DR(NPDR group,n=43)and proliferative DR(PDR group,n=32).In addition,75 patients with simple type 2 diabetes who came to Handan Central Hospital were included as non DR group.The levels of serum circHOMER1,miR-23a-3p,malondialdehyde(MDA),superoxide dismutase(SOD),and reduced glutathione(GSH)were detect-ed.Clinical data of the subjects were collected.The TargetScan website was used to predict the targeting relationship between circHOMER1 and miR-23a-3p.Pearson method was used to analyze the correlation between serum circHOMER1,miR-23a-3p and MDA,SOD,GSH.Univariate and multivariate Logistic regression were used to analyze the influencing factors of progression of DR in type 2 diabetes patients.Receiver operating characteristic(ROC)carve was used to analyze the predictive value of serum circHOMER1 and miR-23a-3p in the progression of DR in patients with type 2 diabetes.Results There was a targeted relationship between circHOMER1 and miR-23a-3p.The serum MDA(28.66±4.52ng/ml)and circHOMER1(1.24±0.16)levels in the DR group were higher than those in the non DR group(16.95±3.27ng/ml,1.02±0.11),while SOD(45.39±7.84U/L),GSH(135.82±21.23μg/mL)and miR-23a-3p(0.88±0.07)levels were lower than those in the non DR group(81.65±11.47U/L,207.44±25.95μg/mL,1.01±0.09),and differences were statistically significant(t=9.813～22.602,all P<0.001).The serum MDA(33.28±4.96ng/ml)and circHOMER1(1.36±0.20)levels in the PDR group were higher than those in the NPDR group(25.23±3.58ng/ml,1.15±0.17),while SOD(34.39±7.15U/L),GSH(113.50±20.17μg/ml)and miR-23a-3p(0.79±0.07)levels were lower than those in the NPDR group(53.27±8.44U/L,152.43±23.99μg/ml,0.94±0.08),and the differences were statistically significant(t=4.906～10.376,all P<0.001).Spearman analysis showed that serum MDA and circHOMER1 were positively correlated with the severity of DR(r=0.533,0.473,all P<0.001),while SOD,GSH,miR-23a-3p were negatively correlated with the severity of DR(r=-0.552,-0.515,-0.529,all P<0.001).Pearson analysis showed that serum circHOMER1 was negatively correlated with miR-23a-3p,SOD,GSH,and positively correlated with MDA(r=-0.475,-0.460,-0.455,0.462,all P<0.001).Serum miR-23a-3p was positively correlated with SOD and GSH,and negatively correlated with MDA(r=0.428,0.437,-0.439,all P<0.001).Logistic regression analysis showed that high MDA,low SOD,low GSH,high circHOMER1,low miR-23a-3p,high FPG and high HbA1c were the risk factors of progression of DR in type 2 diabetes patients(OR=0.214～3.556,all P<0.05).The area under curve(AUC)of serum circHOMER1 and miR-23a-3p alone and jointhy predicting the progression of DR in type 2 diabetes patients were 0.751,0.797 and 0.903 respectively.The combined prediction was higher than that of serum circHOMER1 and miR-23a-3p alone(Z=3.179,2.335,P=0.002,0.020).Conclusion Serum MDA and circHOMER1 levels are higher in DR patients,while serum SOD,GSH and miR-23a-3p levels are lower.Abnormal expression of circHOMER1 and miR-23a-3p in serum is associated with progression of DR and oxidative stress.Combined detection of circHOMER1 and miR-23a-3p in serum can predict the progression of DR in patients with type 2 diabetes.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objective:To evaluate the effectiveness and safety of zoledronic acid in patients with Paget′s disease of bone based on clinical data from a single medical center.Methods:This retrospective study included 24 patients diagnosed with Paget′s disease of bone and treated with zoledronic acid at Peking Union Medical College Hospital between January 2009 and June 2020. Demographic data, clinical symptoms, treatment efficacy, and safety outcomes were collected. The primary efficacy measure was serum alkaline phosphatase(ALP) levels. Treatment was considered effective if ALP levels returned to normal or decreased by more than 75% from baseline in the difference between the ALP level and its normal median value.Results:Among the 24 patients with Paget′s bone disease, the most commonly affected site was the skull(in 17 cases). All patients received a single 5 mg intravenous infusion of zoledronic acid. Serum ALP levels significantly decreased after treatment. Among the 15 patients who completed at least 3 months of follow-up, all achieved treatment success. The median time for serum ALP levels to reach the target was 13.1(9.4, 26.1) weeks. In 12 patients, ALP levels normalized within a medium of 16.9(11.5, 37.3) weeks, and remained stable over a medium follow-up of 4.56(2.42, 5.71) years. The most common side effects were hypocalcemia(21 cases, 87.5%) and flu-like symptoms(17 cases, 70.8%). Seven patients had severe hypocalcemia(serum calcium<1.75 mmol/L), and they had higher baseline levels of ALP, calcium, and phosphorus compared to those with mild hypocalcemia.Conclusions:Zoledronic acid 5 mg intravenous infusion effectively controlled disease activity in patients with Paget′s disease of bone. Generally, Most patients achieved treatment goals within 3-4 months, with sustained remission for a median of 4 years. Hypocalcemia was the most frequent side effect, underscoring the importance of timely calcium and vitamin D supplementation.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

Objectives: Hypoparathyroidism (HP) is a rare endocrine disorder caused by parathyroid hormone (PTH) defi ciency. The PTH is a candidate gene for familial isolated hypoparathyroidism (FIH). This study aimed to investigate the pathogenicity of two novel rare variants (RVs) ofPTH through in vitro functional study. Methods: Targeted next-generation sequencing was used to identify candidate gene mutations. Clinical data were retrospectively collected. Wild-type (WT) PTH was used as a template for site-directed mutagenesis to create mutant eukaryotic expression plasmids, which were transfected into cells. Treated with or without 4-phenylbu tyric acid (4-PBA), the levels of intact PTH (iPTH) and PTH (1-84) were measured by chemiluminescence, and protein expression was assessed using Western blotting. Results: Two patients carrying PTH mutations (c.154G > A: p.Val52Ile, c.270G > T: p.Leu90Phe) were identified.Patient 1, a 45-year-old male, presented with carpal and pedal numbness, muscle cramps, and low serum calcium (1.29 mmol/L). Patient 2, a 12-year-old female, had muscle twitches, convulsions, low calcium (1.50 mmol/L), and iPTH of 4 pg/mL. The iPTH or PTH (1-84) levels in the medium transfected with mutant Val52Ile and Leu90Phe PTH decreased by 31%–38%, and 51%–96% compared to WT (allP < 0.05), which were not rescued by 4-PBA. No significant changes in intracellular PTH expression were observed. Conclusions In this study, two novel RVs of PTH(Val52Ile and Leu90Phe) were identified that may impair hormone synthesis and secretion. Our study has broadened the mutation spectrum of the PTH and shed light on potential mechanisms underlying FIH.

BACKGROUND:Electromyographic biofeedback therapy has demonstrated unique advantages of non-invasive,real-time feedback,personalized treatment and promotion of neuroplasticity,and can promote the recovery of motor function in patients with spinal cord injury.OBJECTIVE:To review the current application status and therapeutic effects of electromyographic biofeedback combined with exercise therapy,robotic exoskeletons,and virtual reality technology in the recovery of motor function after spinal cord injury.METHODS:Relevant literature was retrieved from CNKI and PubMed databases up to May 2024.The search terms included"spinal cord injury,EMG biofeedback,physical therapy,robotic exoskeleton,VR,motor function,exercise"in both English and Chinese.Finally,71 articles were included for review.RESULTS AND CONCLUSION:Mechanisms by which electromyographic biofeedback therapy promotes spinal cord injury rehabilitation include promoting neural plasticity changes,strengthening neuromuscular connections and improving movement patterns.Electromyographic biofeedback,as an emerging tool for treating spinal cord injury,is often used in conjunction with other therapeutic methods,including exercise therapy,robotic exoskeletons,and VR,to promote the recovery of motor function after spinal cord injury.The effectiveness of combination therapy has been significantly improved.However,there are still some problems and challenges,such as the lack of detailed analysis of the mechanism,the lack of large-scale trials that provide strong evidence for combined efficacy,and the limited adaptability of the technology.Future research can focus on these aspects:to improve the personalization and accuracy of electromyographic biofeedback;to develop new rehabilitation equipment and expand the application areas of electromyographic biofeedback combined with more advanced technologies or engineering equipment;to apply electromyographic biofeedback to gait training systems,respiratory training systems,and limb-linkage rehabilitation systems,so as to improve the accuracy of the feedback and the effect of personalized treatment plans.At the same time,the ease of use and comfort of the equipment will be improved.