Objective To explore the clinical effect of transcranial direct current stimulation(tDCS)treatment strategy based on bi-modal balance model on upper limb dysfunction after ischemic stroke.Methods From October,2023 to December,2024,60 patients with ischemic stroke in General Hospital of Ningxia Medi-cal University were randomly divided into control group(n=30)and experimental group(n=30).Both groups received basic rehabilitation,the control group received tDCS based on the theory of interhemispheric competi-tion model,and the experimental group received tDCS based on the theory of bimodal equilibrium model,for four weeks.Before and after intervention,the effect of both groups was evaluated using Fugl-Meyer Assessment-Upper Extremities(FMA-UE),modified Ashworth Scale(MAS),Action Research Arm Test(ARAT)and modi-fied Barthel Index(MBI).Neurophysiological parameters such as cortical latency(CL)and central motor conduc-tion time(CMCT)were detected and correlated analysis was performed.Results Two cases in the control group and one in the experimental group dropped down.After intervention,the scores of FMA-UE,ARAT and MBI increased in both groups(|t|>13.748,P<0.001),and the above scores were higher in the experimental group than in the control group(|t|>2.321,P<0.05);the MAS grade of the elbow flexor muscle group improved in the experimental group(|Z|=2.095,P<0.05).The CL and CMCT in both groups de-creased(|t|>2.752,P<0.001),and they were better in the experimental group than in the control group(|t|>2.082,P<0.05).There was a correlation between FMA-UE and CMCT(r=-0.433,P<0.05).Conclusion tDCS based on bimodal balance model can improve upper limb dysfunction more effectively in patients with ischemic stroke.

BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

Objective To explore the clinical effect of transcranial direct current stimulation(tDCS)treatment strategy based on bi-modal balance model on upper limb dysfunction after ischemic stroke.Methods From October,2023 to December,2024,60 patients with ischemic stroke in General Hospital of Ningxia Medi-cal University were randomly divided into control group(n=30)and experimental group(n=30).Both groups received basic rehabilitation,the control group received tDCS based on the theory of interhemispheric competi-tion model,and the experimental group received tDCS based on the theory of bimodal equilibrium model,for four weeks.Before and after intervention,the effect of both groups was evaluated using Fugl-Meyer Assessment-Upper Extremities(FMA-UE),modified Ashworth Scale(MAS),Action Research Arm Test(ARAT)and modi-fied Barthel Index(MBI).Neurophysiological parameters such as cortical latency(CL)and central motor conduc-tion time(CMCT)were detected and correlated analysis was performed.Results Two cases in the control group and one in the experimental group dropped down.After intervention,the scores of FMA-UE,ARAT and MBI increased in both groups(|t|>13.748,P<0.001),and the above scores were higher in the experimental group than in the control group(|t|>2.321,P<0.05);the MAS grade of the elbow flexor muscle group improved in the experimental group(|Z|=2.095,P<0.05).The CL and CMCT in both groups de-creased(|t|>2.752,P<0.001),and they were better in the experimental group than in the control group(|t|>2.082,P<0.05).There was a correlation between FMA-UE and CMCT(r=-0.433,P<0.05).Conclusion tDCS based on bimodal balance model can improve upper limb dysfunction more effectively in patients with ischemic stroke.

BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

OBJECTIVE To investigate whether electroacupuncture(EA)ameliorates abnormal trigeminal neuralgia(TN)orofacial pain and anxiety-like behavior by altering synaptic plasticity in the hippocampus CA1.METHODS A mouse infraorbital nerve transection model(pT-ION)of neuropathic pain was established,and EA or sham EA was used to treat ipsilateral acu-puncture points(GV20-Baihui and ST7-Xia-guan).Golgi-Cox staining and transmission elec-tron microscopy(TEM)were administrated to observe the changes of synaptic plasticity in the hippocampus CA1.RESULTS Stable and per-sistent orofacial allodynia and anxiety-like behav-iors induced by pT-ION were related to changes in hippocampal synaptic plasticity.Golgi stain-ings showed a decrease in the density of dendritic spines,especially mushroom-type dendritic spines,in hippocampal CA1 neurons of pT-ION mice.TEM results showed that the density of synapses,membrane thickness of the postsynap-tic density,and length of the synaptic active zone were decreased,whereas the width of the synap-tic cleft was increased in pTION mice.EA attenu-ated pT-ION-induced orofacial allodynia and anx-iety-like behaviors and effectively reversed the abnormal changes in dendritic spines and syn-apse of the hippocampal CA1 region.CONCLU-SION EA modulates synaptic plasticity of hippo-campal CA1 neurons,and reduces abnormal oro-facial pain and anxiety-like behavior,providing evidence for a TN treatment strategy.