Objective:To observe the effect of intensified heel anti-gravity posture stability training on the gait of stroke survivors.Methods:Thirty-six hemiplegic stroke survivors were randomly divided into a control group and an experimental group, each of 18. Both groups received conventional rehabilitation treatment (including limb positioning, limb movement training and conventional walking training), while the experimental group was additionally provided with 30 minutes of intense heel anti-gravity posture stability training 5 days a week for 4 weeks. Before and after the treatment, the subjects′ walking speed, stride frequency, step length, peak knee flexion angle and peak hip flexion angle were documented using three-dimensional gait analysis with a movement training system.Results:The average walking speed, stride rate, step length, peak hip flexion and peak knee flexion of both groups had improved significantly after the treatments. But the average walking speed [(0.46±0.06)m/s], step length [(85.05±6.68)cm], peak hip flexion angle [(34.80±2.80)°] and peak knee flexion angle [(40.55±3.58)°] of the treatment group were significantly better than those of the control group.Conclusions:Intensified heel anti-gravity posture stability training can significantly improve the walking speed, step length, hip flexion and knee flexion of hemiplegic stroke survivors.

The Expert Consensus on Clinical Application of Qinbaohong Zhike Oral Liquid in Treatment of Acute Bronchitis and Acute Attack of Chronic Bronchitis （GS/CACM 337-2023） was released by the China Association of Chinese Medicine on December 13^th， 2023. This expert consensus was developed by experts in methodology， pharmacy， and Chinese medicine in strict accordance with the development requirements of the China Association of Chinese Medicine （CACM） and based on the latest medical evidence and the clinical medication experience of well-known experts in the fields of respiratory medicine （pulmonary diseases） and pediatrics. This expert consensus defines the application of Qinbaohong Zhike oral liquid in the treatment of cough and excessive sputum caused by phlegm-heat obstructing lung， acute bronchitis， and acute attack of chronic bronchitis from the aspects of applicable populations， efficacy evaluation， usage， dosage， drug combination， and safety. It is expected to guide the rational drug use in medical and health institutions， give full play to the unique value of Qinbaohong Zhike oral liquid， and vigorously promote the inheritance and innovation of Chinese patent medicines.

Objective:To investigate the effect of aucubin(AU)on mitochondrial autophagy in the hippocampus of ischemic stroke(IS)rats by regulating the pten-induced kinase protein 1(PINK1)/cytoplasmic E3-ubiquitin ligase(Parkin)signaling pathway.Methods:The IS rat model was established by middle cerebral artery occlusion(MCAO),and was randomly divided into IS group,low-dose AU group(AU-L),medium-dose AU group(AU-M),high-dose AU group(AU-H),and high-dose AU combined with 3-MA group(AU-H+3-MA).The rats without liga-tion were used as the Sham surgery group.Zea Longa score was used to evaluate the neurological function of rats.TTC staining was used to detect the percentage of cerebral infarction volume.The microstructures of mitochondria were observed by transmission electron microscopy,and the changes of autophagy protein-microtubule associated protein light chain 3B(LC3B)and p62 were detected by immunohistochemistry.Hippocampal apoptosis was detected by TUNEL.PINK1/Parkin-related protein expression in hippocampus was detected by Western blot.Results:Neurological function score of IS rats was increased(P＜0.05),cerebral infarction was observed by TTC staining,the expression of mito-chondrial autophagy protein p62 in hippocampus was up-regulated(P＜0.05),the expression of LC3B was down-regu-lated(P＜0.05),the number of autophagosomes was decreased(P＜0.05),and apoptosis in hippocampus was in-creased(P＜0.05),the expression of PINK1 and ARKIN protein in hippocampus was down-regulated(P＜0.05).After AU intervention,the neural function score of rats was decreased,the percentage of cerebral infarction volume was reduced,the positive expression of p62 in hippocampus was down-regulated(P＜0.05),the positive expression of LC3B was up-regulated(P＜0.05),and the number of autophagosomes was increased(P＜0.05),the apoptosis of hippocampus was decreased(P＜0.05),and the expression of PINK1 and ARKIN protein in hippocampus was in-creased(P＜0.05).3-MA blocked the therapeutic effect of AU and aggravated the nerve injury in rats.Conclusion:AU promotes hippocampal mitochondrial autophagy and improves neurological damage in IS rats by activating the PINK1/Parkin signaling pathway.

Objective:To investigate the effect of aucubin(AU)on mitochondrial autophagy in the hippocampus of ischemic stroke(IS)rats by regulating the pten-induced kinase protein 1(PINK1)/cytoplasmic E3-ubiquitin ligase(Parkin)signaling pathway.Methods:The IS rat model was established by middle cerebral artery occlusion(MCAO),and was randomly divided into IS group,low-dose AU group(AU-L),medium-dose AU group(AU-M),high-dose AU group(AU-H),and high-dose AU combined with 3-MA group(AU-H+3-MA).The rats without liga-tion were used as the Sham surgery group.Zea Longa score was used to evaluate the neurological function of rats.TTC staining was used to detect the percentage of cerebral infarction volume.The microstructures of mitochondria were observed by transmission electron microscopy,and the changes of autophagy protein-microtubule associated protein light chain 3B(LC3B)and p62 were detected by immunohistochemistry.Hippocampal apoptosis was detected by TUNEL.PINK1/Parkin-related protein expression in hippocampus was detected by Western blot.Results:Neurological function score of IS rats was increased(P＜0.05),cerebral infarction was observed by TTC staining,the expression of mito-chondrial autophagy protein p62 in hippocampus was up-regulated(P＜0.05),the expression of LC3B was down-regu-lated(P＜0.05),the number of autophagosomes was decreased(P＜0.05),and apoptosis in hippocampus was in-creased(P＜0.05),the expression of PINK1 and ARKIN protein in hippocampus was down-regulated(P＜0.05).After AU intervention,the neural function score of rats was decreased,the percentage of cerebral infarction volume was reduced,the positive expression of p62 in hippocampus was down-regulated(P＜0.05),the positive expression of LC3B was up-regulated(P＜0.05),and the number of autophagosomes was increased(P＜0.05),the apoptosis of hippocampus was decreased(P＜0.05),and the expression of PINK1 and ARKIN protein in hippocampus was in-creased(P＜0.05).3-MA blocked the therapeutic effect of AU and aggravated the nerve injury in rats.Conclusion:AU promotes hippocampal mitochondrial autophagy and improves neurological damage in IS rats by activating the PINK1/Parkin signaling pathway.

Objective:To observe the effect of intensified heel anti-gravity posture stability training on the gait of stroke survivors.Methods:Thirty-six hemiplegic stroke survivors were randomly divided into a control group and an experimental group, each of 18. Both groups received conventional rehabilitation treatment (including limb positioning, limb movement training and conventional walking training), while the experimental group was additionally provided with 30 minutes of intense heel anti-gravity posture stability training 5 days a week for 4 weeks. Before and after the treatment, the subjects′ walking speed, stride frequency, step length, peak knee flexion angle and peak hip flexion angle were documented using three-dimensional gait analysis with a movement training system.Results:The average walking speed, stride rate, step length, peak hip flexion and peak knee flexion of both groups had improved significantly after the treatments. But the average walking speed [(0.46±0.06)m/s], step length [(85.05±6.68)cm], peak hip flexion angle [(34.80±2.80)°] and peak knee flexion angle [(40.55±3.58)°] of the treatment group were significantly better than those of the control group.Conclusions:Intensified heel anti-gravity posture stability training can significantly improve the walking speed, step length, hip flexion and knee flexion of hemiplegic stroke survivors.

OBJECTIVES: Stroke patients may have various sensory-motor disorders, such as spasticity, muscle weakness or sensory damage. Spasticity affects 20% to 40% of stroke patients. Patients with spasticity may have problems such as pain, motor function damage, and the decreased range of motion, which leads to decline of activity and quality of daily life. Extracorporeal shock wave therapy (ESWT) is a technique that can improve post-stroke spasticity. Whole body vibration (WBV), as a passive neuromuscular muscle stimulation technique, can improve the posture control, muscle strength, and muscle work of different people. At present, there are still few studies using WBV combined with ESWT for the treatment of hemiplegic patients with stroke. This study aims to explore the effects of WBV combined with ESWT on spasticity of the affected lower limb and gait function in stroke patients. METHODS: From March 2020 to March 2021, 50 hemiplegic patients with stroke were treated in the Department of Rehabilitation Medicine of the First Hospital of Changsha and they were assigned into a control group and a combined group, 25 cases per group. Both groups carried out conventional treatment, while the control group undertook the ESWT and fake WBV based on conventional treatment, and the combined group undertook ESWT after WBV and conventional treatment. Modified Ashworth Scale (MAS), Lower Extremity portion of the Fugl-Meyer Motor Assessment (FMA-LE), Berg Balance Scale (BBS), and parameters of three-dimensional gait analysis including kinematic parameters (peak value of hip flexion and knee flexion) and spatiotemporal parameters (velocity, cadence and stride length) were assessed before and after 4-week treatment between the 2 groups. RESULTS: After 4 weeks of treatment, MAS scores in 2 groups were lower than before (both P<0.05), and the combined group was lower than the control group (P<0.001); BBS and FMA-LE scores were higher than those before treatment (both P<0.05), and the combined group was higher than the control group (both P<0.001); in the control group, the walking speed, stride frequency, and stride length were higher than those before treatment (all P<0.05), and there was no significant difference between the peak value of flexion hip and peak value of flexion knee (both P<0.05); the peak value of hip flexion, peak value of knee flexion, step speed, step frequency, and stride length in the combined group were higher than those before treatment (all P<0.05), and were higher than those in control group (P<0.05 or P<0.001). CONCLUSIONS WBV combined with ESWT can improve the spasticity and motor function of the affected lower extremity, balance, and gait in hemiplegic patients with stroke.
Extracorporeal Shockwave Therapy ; Gait ; Hemiplegia/therapy* ; Humans ; Muscle Spasticity/therapy* ; Stroke/complications* ; Stroke Rehabilitation/methods* ; Treatment Outcome ; Vibration/therapeutic use*

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.

Objective To establish a cell model mimicking Alzheimer's disease (AD) by knocking down SORL1 gene and compare the viability, apoptosis, and expressions of tumor necrosis factor-α( TNF-α) and interleukin-1β(IL-1β) in this model with a traditional Alzheimer's disease cell model. Methods A traditional cell model of AD was established by inducing N2a cells with Aβ25-35, and the optimal Aβ25-35 concentration was determined by assessing the cell viability changes. Another cell model of AD was established by transfecting N2a cells with SORL1-shRNA lentiviral vector, and SORL1 expression in the transfected cells were detected using Western blotting and qRT-PCR. With wild-type N2a cells without any treatment and cells transfected with a scramble shRNA as the control groups, the two cell models were examined for cell viability with MTT assay, cell apoptosis with flow cytometry, and TNF-αand IL-1βlevels in the culture supernatant with ELISA. Results The two cell models of AD showed obviously decreased viability and increased cell apoptosis compared with the untreated control cells or cells transfected with a scramble shRNA (P<0.05); no significant difference was found in the cell viability and apoptosis rate between the two AD cell models or between the two control groups (P>0.05). Significantly increased expressions of TNF-αand IL-1βwere observed in both of the two cell models compared with their respective control groups (P<0.05) without significant differences between the two cell models or between the two control groups (P>0.05). Conclusion A new AD cell model similar to Aβ25-35-induced AD model can be established by SORL1 knockdown in N2a cells.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.