The machine learning is used increasingly and widely in acupuncture prescription optimization, intelligent treatment and precision medicine, and has obtained a certain achievement. But, there are still some problems remained to be solved such as the poor interpretability of the model, the inconsistency of data quality of acupuncture research, and the clinical application of constructed models. Researches in future should focus on the acquisition of high-quality clinical and experimental data sets, take various machine learning algorithms as the basis, and construct professional models to solve various problems, so as to drive the high-quality development of acupuncture research.
Acupuncture Therapy/trends* ; Machine Learning ; Humans ; Algorithms

Objective To study the requirement of exogenous phosphorus for 2-year-old and 3-year-old ginseng seedings.Methods Two-and three-year-old ginsengs were used as experimental materials.Calcium superphosphate and phosphorus-free Hoagland solution were used as fertilizer,and the concentrations of P2O5 were set to be 0 mmol·L-1,0.5 mmol·L-1,1.5 mmol·L-1,3 mmol·L-1,6 mmol·L-1,8 mmol·L-1,respectively.The effects of different concentrations of phosphorus fertilizer on agronomic indexes,photosynthetic characteristics and accumulation of ginsenosides Rg1,Rb1 and Re were studied.Results The plant height,stem diameter,root weight,leaf area,relative content of chlorophyll,net photosynthetic rate and total saponins content of different year-old panax ginseng were significantly increased by applying phosphorus at 1.5-3.0 mmol·L-1.Among them,compared with the phosphorus-free group,the root weight of second-year ginseng was increased by 16％and the saponin content was increased by 24％;the root weight of third-year ginseng was increased by 89％and the saponin content was increased by 132％.The appropriate application rate of phosphorus fertilizer(phosphorus pentoxide)during the growth of second and third year ginseng was 26.6 mg and 53.3 mg of plant,respectively.Conclusion External application of suitable concentration of phosphorus fertilizer can enhance the external morphological characteristics of ginseng,improve photosynthetic physiological properties and increase the content of active ingredients.

Objective To investigate the effects of dexmedetomidine on the proliferation and auto-phagy of human colon cancer cells.Methods In experiment 1,human colon cancer cells LoVo and HCT116 were selected and divided into eight groups:LoVo-1 group(group L0-1),LoVo+dexmedetomi-dine 1 nmol/L-1 group(group L1-1),LoVo+dexmedetomidine 10 nmol/L-1 group(group L10-1),LoVo+dexmedetomidine 100 nmol/L-1 group(group L100-1),HCT116-1 group(group H0-1),HCT116+dexmedetomidine 1 nmol/L-1 group(group H1-1),HCT116+dexmedetomidine 10 nmol/L-1 group(group H10-1)and HCT116+dexmedetomidine 100 nmol/L-1 group(group H100-1).The cell proliferation rate was detected by CCK-8 method 24 and 48 hours after drug treatment.The cells were collected 24 hours after drug treatment,and the contents of microtubule-associated protein 1 light chain 3(LC3)-Ⅱ and autophagy associated protein Beclin-1 were detected by Western blot method.In experiment 2,LoVo and HCT116 were selected and divided into four groups:LoVo-2 group(group L0-2),LoVo+dexmedetomidine 10 nmol/L-2 group(group L10-2),HCT116-2 group(group H0-2)and HCT116+dexmedetomidine 10 nmol/L-2 group(group H10-2).Cells were collected 24 hours after drug treatment,LC3 protein expression was observed by immunofluorescence method,and the positive rate of LC3 site was calculated.The autophagosomes were col-lected and observed by transmission electron microscopy 24 hours after drug treatment.Results In experi-ment 1,the cell proliferation rate in groups L10-1 and L100-1 was significantly lower than that in groups L0-1 and L1-1 24 and 48 hours after drug treatment,the protein content of LC3-Ⅱ and Beclin-1 was signifi-cantly higher than that in groups L0-1 and L1-1 24 hours after drug treatment(P＜0.05).The cell prolifer-ation rate in groups H10-1 and H100-1 was significantly lower than that in groups H0-1 and H1-1 24 and 48 hours after drug treatment,and the protein content of LC3-Ⅱ and Beclin-1 was significantly higher than that in groups H0-1 and H1-1 24 hours after drug treatment(P＜0.05).In experiment 2,compared with group L0-2,the positive rate of LC3 site in group L10-2 was significantly increased 24 hours after drug treatment(P＜0.05).Compared with group H0-2,the positive rate of LC3 site in group H10-2 was significantly in-creased 24 hours after drug treatment(P＜0.05).Groups L0-2 and H0-2 have intact cell membranes and clear nuclei.The cell membrane in groups L10-2 and H10-2 was damaged,the arrangement of organelles was disordered,and a large number of autophagosomes and autophagosomes were visible.Conclusion Dexmedetomidine may inhibit the proliferation of colon cancer cells by inducing autophagy.

Sha （痧） is an acute infectious disease characterised by the appearance of rashes on the skin， caused by exposure to epidemic toxin and pestilent qi. Sha Zhang Yu Heng （《痧胀玉衡》） discussed the treatment principles and methods， and listed collateral bloodletting as one of the main treatments. Through organizing the articles and proved cases， we found that the author believes Sha （痧） is caused by epidemic pathogen， belonging to heat toxin with rapid changes， so timely treatment for qi and blood simultaneously could achieve the effect of transforming qi into defensive qi. Sha Zhang Yu Heng focuses on patient's position during treatmet， the material of the needle， the site of treatment， the quantum of stimulation and the operation of the contraindications and other essentials. According to the depth of the disease location， use traditional Chinese herbal medicine， scraping together to identify the root of the disease. In addition， diet suggestions for the prevention of the recrudescence of disease are also described in detail.

Objective:To evaluate the effect of esketamine on learning and memory function after chronic stress and the signaling pathway of N-methyl-D-aspartate receptor (NMDAR)-calmodulin-dependent protein kinase type 2 (CaMKⅡ)-cAMP-responsive element-binding protein (CREB) in the hippocampus of developing rats.Methods:Sixty clean-grade healthy Sprague-Dawley rats of either sex, aged 7 days, weighing 10-15 g, were divided into 3 groups ( n=20 each) using a random number table method: control+ normal saline group (CN group), chronic stress+ normal saline group (NS group), and chronic stress+ esketamine group (ES group). A chronic stress model was established using a chronic unpredictable stress method. After the end of stress stimulation, esketamine 10 mg/kg was intraperitoneally injected once a day for 7 consecutive days in ES group, and the equal volume of normal saline was given instead in NS group. Y maze test and Morris water maze test were used to assess the learning and memory function after intraperitoneal administration. Venous blood samples were obtained to measure the serum cortisol and reactive oxygen species (ROS) concentrations by enzyme-linked immunosorbent assay. The animals were then sacrificed under anesthesia, the brain was removed and the hippocampal tissue was isolated for examination of the pathological changes in the hippocampal CA1 region and for determination of the ratios of phosphorylated NMDAR (p-NMDAR)/NMDAR, phosphorylated CaMKII (p-CaMKⅡ)/CaMKⅡ, and phosphorylated CREB (p-CREB)/CREB (by Western blot). Results:Compared with CN group, the time spent in the novel arm was significantly shortened, the number of entries into the novel arm was reduced, the escape latency was prolonged, the number of crossing the original platform was reduced, the serum cortisol and ROS concentrations were increased, the p-NMDAR/NMDAR ratio, p-CaMKⅡ/CaMKⅡ ratio and p-CREB/CREB ratio were decreased ( P<0.05), and the pathological changes of neurons were marked in NS group. Compared with NS group, the time spent in the novel arm was significantly prolonged, the number of entries into the novel arm was increased, the escape latency was shortened, the number of crossing the original platform was increased, the serum cortisol and ROS concentrations were decreased, the p-NMDAR/NMDAR ratio, p-CaMKⅡ/CaMKⅡ ratio and p-CREB/CREB ratio were increased ( P<0.05), and the pathological changes of neurons were significantly attenuated in ES group. Conclusions:Esketamine can improve the learning and memory function after chronic stress in developing rats, and the mechanism may be related to reduction of oxidative stress and enhancement of the activity of hippocampal NMDAR-CaMKII-CREB signaling pathway.

Objective To investigate the effect of resveratrol(Rsv)on inhibiting miR-149-5p-mediated ferroptosis and impro-ving lipopolysaccharide(LPS)-induced cardiomyocyte(H9C2)injury.Methods Different concentrations of Rsv were used to treat H9C2 cells,followed by LPS stimulation to observe the effect of Rsv on LPS-induced injury in H9C2 cells.The H9C2 cells were divided into different groups,including the Control group,LPS group,LPS+Rsv group,LPS+miRNA-inhibitor-NC group,LPS+miR149-5p-inhibitor group,and LPS+miR149-5p-inhibitor+Rsv group.CCK-8 assay was used to detect cell viability,and a kit was used to measure changes in lactate dehydrogenase(LDH),glutathione(GSH),and malondialdehyde(MDA)release in H9C2 cells.DCFH-DA fluorescent probe was used to determine the level of reactive oxygen species(ROS)in H9C2 cells.Iron ion colorimetry was used to observe changes in Fe2+content in cardiomyocytes,and RT-qPCR was used to detect the expression of miR-149-5p in cells.Results Rsv significantly reduced LPS-induced injury in H9C2 cells.Compared with the LPS group,the Rsv+LPS group showed in-creased cell viability,reduced LDH secretion,increased GSH release,reduced lipid ROS generation,decreased Fe2+content,reduced MDA release,and increased miR-149-5p expression.Compared with the LPS+miR-149-5p-inhibitor group,the LPS+miR-149-5p-inhibitor+Rsv group showed increased cell viability,reduced LDH content,increased GSH,reduced ROS production,re-duced lipid peroxidation and iron accumulation,and increased miR-149-5p expression.Conclusion Rsv may inhibit ferroptosis by upregulating miR-149-5p expression and thus alleviate LPS-induced injury in H9C2 cells.

Objective:To evaluate the role of microRNA-149-5p (miR-149-5p) in resveratrol-induced reduction of lipopolysaccharide (LPS)-induced cardiomyocyte injury in rats.Methods:Rat cardiomyocyte cell line H9C2 was cultured and then divided into 5 groups ( n=27 each) using a random number method: control group (C group), LPS group, resveratrol group (RSV group), miR149-5p inhibitor negative control group (LRN group), and miR149-5p inhibitor group (LRI group). A cardiomyocyte injury model was prepared by incubating cells with culture medium containing 10 μg/ml LPS for 24 h. RSV group was incubated with resveratrol (final concentration of 10 μmol/L) for 24 h, followed by incubation with culture medium containing 10 μg/ml LPS for another 24 h. LRN group and LRI group were transfected with miR149-5p inhibitor negative control and miR149-5p inhibitor, respectively, and then the other treatments were similar to those previously described in RSV group. The cell viability was measured by CCK-8 assay, the apoptosis rate by flow cytometry, the concentration of lactate dehydrogenase (LDH) and content of glutathione (GSH) in the supernatant by microplate method, the content of malondialdehyde (MDA) by TBA reaction method, the activity of superoxide dismutase (SOD) by WST-1 method, the level of reactive oxygen species (ROS) by DCFH-DA fluorescent probe, the concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the supernatant by enzyme-linked immunosorbent assay, and the expression of miR-149-5p by quantitative real-time polymerase chain reaction. Results:Compared with C group, the expression of miR-149-5p was significantly down-regulated, the cell viability was decreased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were increased, and the GSH content and SOD activity were decreased in LPS group ( P<0.05). Compared with LPS group, the expression of miR-149-5p was significantly up-regulated, the cell viability was increased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were decreased, and the GSH content and SOD activity were increased in RSV group ( P<0.05). Compared with RSV group or LRN group, the expression of miR-149-5p was significantly down-regulated, the cell viability was decreased, the concentrations of LDH, TNF-α and IL-6 in supernatant, apoptosis rate, ROS level and MDA content were increased, and the GSH content and SOD activity were decreased in LRI group ( P<0.05). Conclusions:The mechanism by which resveratrol alleviates LPS-induced cardiomyocyte injury is associated with the up-regulation of miR-149-5p expression and inhibition of cell apoptosis, oxidative stress and inflammatory responses in rats.

Objective:To evaluate the effect of dexmedetomidine on the hippocampal brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrκB) signaling pathway in a rat model of cerebral ischemia-reperfusion (I/R).Methods:Forty-five clean-grade healthy Sprague-Dawley rats, half male and half female, aged 5-6 months, weighing 200-250 g, were divided into 3 groups ( n=15 each) using a random number table method: sham operation group (group S), cerebral I/R group (group I/R), and dexmedetomidine + I/R group (group Dex). A rat model of cerebral I/R injury was established by occluding the middle cerebral artery for 90 min followed by restoring perfusion. In group Dex, dexmedetomidine 50 μg/kg was intraperitoneally injected at 30 min before ischemia, while the equal volume of normal saline was intraperitoneally injected in S and I/R groups. Neurological deficit scores were evaluated at 12 h of reperfusion. The rats were anesthetized and sacrificed, and the hippocampus was isolated for determination of the percentage of cerebral infarct size (by TTC method), expression of BDNF and TrκB (by Western blot), and expression of BDNF mRNA and TrκB mRNA (by real-time polymerase chain reaction) and for microscopic examination of cell apoptosis (by TUNEL method). Results:Compared with group S, the neurological deficit scores and percentage of cerebral infarct size were significantly increased, the number of apoptotic hippocampal neurons was increased, and the expression of BDNF and TrκB protein and mRNA was down-regulated in I/R and Dex groups ( P<0.05). Compared with group I/R, the neurological deficit scores and percentage of cerebral infarct size were significantly decreased, the number of apoptotic hippocampal neurons was reduced, and the expression of BDNF and TrκB protein and mRNA was up-regulated in group Dex ( P<0.05). Conclusions:The mechanism by which dexmedetomidine alleviates cerebral I/R injury may be related to activating hippocampal BDNF/TrκB signaling pathways in rats.

Lung cancer, particularly non-small cell lung cancer (NSCLC) which contributes more than 80% to totally lung cancer cases, remains the leading cause of cancer death and the 5-year survival is less than 20%. Continuous understanding on the mechanisms underlying the pathogenesis of this disease and identification of biomarkers for therapeutic application and response to treatment will help to improve patient survival. Here we found that a molecule known as DUSP10 (also known as MAPK phosphatase 5) is oncogenic in NSCLC.Overexpression of DUSP10 in NSCLC cells resulted in reduced activation of ERK and JNK, but increased activation of p38, which was associated with increased cellular growth and migration. When inoculated in immunodeficient mice, the DUSP10-overexpression NSCLC cells formed larger tumors compared to control cells. The increased growth of DUSP10-overexpression NSCLC cells was associated with increased expression of tumor-promoting cytokines including IL-6 and TGFβ. Importantly, higher DUSP10 expression was associated with poorer prognosis of NSCLC patients. Therefore, DUSP10 could severe as a biomarker for NSCLC prognosis and could be a target for development of therapeutic method for lung cancer treatment.

Objective:To observe any effect of low-frequency whole body resonant stimulation on the ba-lance and walking ability of hemiplegic stroke survivors.Methods:Sixty-six stroke survivors with hemiplegia were randomly divided into a low-frequency resonance training group, a high-frequency vibration training group and a control group, each of 22. All received routine exercise training at individualized intensities. All three groups underwent five 1-minute cycles of 7Hz, 15Hz or 1Hz stimulation twice a day, five days a week for eight weeks. Before and after the intervention, balance and walking ability were evaluated using the Berg Balance Scale, the timed up and go test and a 10m walking test. Step length, step frequency and step speed were also measured.Results:There were no significant differences among the three groups before the training. Afterward, significant improvement was observed in all of the groups in terms of all of the measurements. The average results of the low-frequency resonance training group were at that point significantly better than the other two groups′ averages, while the high-frequency vibration training group′s results were superior to those of the control group.Conclusion:Resonance training at 7Hz is the most effective in improving the balance and walking ability of stroke survivors with hemiplegia.