With acupuncture depth as a perspective, some related issues are discussed in this paper. Firstly, the possible reasons of divergence on needling depth are explained. Secondly, by literature retrieval, the advantages and disadvantages of the clinical efficacy of deep needling and shallow needling are explored, and the essential value of shallow needling is emphasized in promoting acupuncture. Thirdly, due to the placebo acupuncture that led to the controversy of the curative effect of acupuncture, it is crucial to establish a method of modern system of scientific research which should be suitable for the development of acupuncture. Finally, the "cun" in acupuncture is inappropriate to transform into millimeter, and the standardization of acupuncture should focus on the improvement of curative efficacy. From the acupuncture depth, it is clear that there are plenty of problems in acupuncture, which could not only limit the development of acupuncture, but also affect the future of acupuncture.
Acupuncture Points ; Acupuncture Therapy ; instrumentation ; methods ; Humans ; Needles

Charcot-Marie-Tooth Disease ; Child, Preschool ; Humans ; Male

The paper aimed to evaluate the effects of lead stress on photosynthetic performance and ginsenoside content in ginseng (Panax ginseng). To accomplish this, three years old ginseng were cultivated in pot and in phytotron with different concentrations of lead, ranging from 0 to 1000 mg x kg(-1) soil for a whole growth period (about 150 days). The photosynthetic parameters in leaves and ginsenoside content in roots of ginseng were determined in green fruit stage and before withering stage, respectively. In comparison with the control, net photosynthetic rate and SPAD value in ginseng leaves cultivated with 100 and 250 mg x kg(-1) of lead changed insignificantly, however, ginseng supplied with 500 and 1 000 mg x kg(-1) of lead showed a noticeably decline in the net rate of photosynthesis and SPAD value (P < 0.05), the lowest net photosynthetic rate and SPAD value showed in the treatment supplied with 1 000 mg x kg(-1) of lead, with decline of 57.8%,11.0%, respectively. Total content of ginsenoside in ginseng roots cultivated with 100 mg x kg(-1) of lead showed insignificantly change compared to the control, but the content increased remarkably in treatments supplied with 250, 500, 1 000 mg x kg(-1) of lead (P < 0.05), and highest content appeared in these ginsengs exposed to 1000 mg x kg(-1) of lead. The net photosynthetic rate and SPAD value in leaves of ginseng both showed significantly negative linear correlations with lead stress level (P < 0.01), and significant positive linear correlations between total content of ginsenoside and lead concentration was also observed (P < 0.05). These results strongly indicate that exposing to high level of lead negatively affects photosynthetic performance in ginseng leaves, but benefits for accumulation of secondary metabolism (total content of ginsenoside) in ginseng root.
Ginsenosides ; analysis ; metabolism ; Lead ; pharmacology ; Panax ; chemistry ; drug effects ; growth & development ; metabolism ; Photosynthesis ; drug effects ; Plant Leaves ; chemistry ; drug effects ; growth & development ; metabolism ; Spectrophotometry

Objective To investigate the correlation of plasma interleukin ( IL)-17 level and IL-17 receptor (IL-17R) expression in the thymus of patients with myasthenia gravis (MG).Methods The blood samples of 63 patients (38 with glucocorticoid treatment, 25 with thymus removal) who admitted to Henan Provincial People′s Hospital between 2010 and 2014 were collected at three different stages: pre-treatment, 1 week post-treatment and 1 month post-treatment.The blood samples of 42 healthy controls were also collected.Enzyme linked immunosorbent assay was used to evaluate the levels of IL-17 in plasma.Twenty-five thymus tissues from MG patients and another 12 thymus tissues from patients with congenital heart disease who had surgery therapy were also collected.Reverse transcription polymerase chain reaction was used to evaluate the mRNA levels of IL-17R.The possible correlation between the expression of IL-17 and IL-17R with MG was analyzed.Results Before treatment, the levels of IL-17 in the plasma were much higher in all the MG patients ( both ocular and generalized) when compared to the healthy controls ( controls (3.2 ±0.7) pg/ml, MG patients (8.5 ±1.7) pg/ml, t =2.450, P <0.01; generalized type patients (9.7 ±1.4) pg/ml, t =2.532, P <0.01).In the patients with glucocorticoid treatment, IL-17 levels began to reduce after 1 week treatment and a statistically significant difference was found when compared to the pre-treatment samples (pre-treatment (8.3 ±1.2) pg/ml, 1 week after treatment (6.3 ±0.7) pg/ml, t=2.052, P<0.05) and healthy controls (t =1.933, P<0.05).One month after the glucocorticoid treatment, the levels of IL-17 decreased to the normal level (1 month after treatment (3.9 ±0.6) pg/ml, t=2.630, P <0.01, compared to the pre-treatment; t =1.395, P >0.05, compared to the healthy controls).In the surgery therapy cases, the IL-17 levels were also reduced after the thymus removal ( pre-surgery (8.8 ±1.4) pg/ml, 1 week after surgery (5.3 ±0.7) pg/ml, t=1.950, P<0.05;1 month after surgery (3.0 ±0.4) pg/ml, t=2.683, P<0.01).In the thymus tissues of the MG patients, the mRNA levels of IL-17R were much higher than that of the controls ( relative level 2.31 folds, t =2.682, P <0.01).Meanwhile, a positive correlation was found between the plasma IL-17 levels and the relative IL-17R levels in thymus tissues ( r =0.945 4, P <0.01 ).Furthermore, IL-17 was positively correlated with quantitative myasthenia gravis scores (QMGS) either pre-treatment (r =0.798 1, P <0.01) or post-treatment (r=0.906 5, P<0.01).And IL-17R was positively correlated with QMGS pre-treatment (r=0.775 5, P<0.01).Conclusions IL-17 is increased in the plasma of MG patients (both ocular and generalized) , and is decreased upon the glucocorticoid treatment or surgery therapy, suggesting that it can be used as a parameter to determine the therapeutic effects.IL-17R is increased in the thymus tissues of MG patients, suggesting that it can potentially be used as a pathological diagnosis parameter.

Child ; Child, Preschool ; Female ; Follicle Stimulating Hormone ; blood ; Gonadotropins ; blood ; Humans ; Infant ; Infant, Newborn ; Male ; Sex Factors ; Time Factors

T cell immune receptor with Ig and ITIM domains (TIGIT), a promising new target in cancer immunotherapy, plays a critical role in limiting adaptive and innate immunity against tumors. The extracellular domain of human TIGIT was used to immune BALB/c mice, and a new anti-human TIGIT chimeric antibody (c7D3) was developed. The mice in this study were used in accordance with the international guidelines for the care and use of laboratory animals, and the animal study was approved by the Institutional Animal Ethics Committee of AbMax Biotechnology. The biological activity of c7D3 was studied. The results showed that c7D3 exhibited high affinity for TIGIT and effectively inhibited the interaction between TIGIT and its ligands. Cell-based assays indicated that c7D3 induced strong luciferase signaling in TIGIT/CD155 signaling reporter assay and enhanced cytokine secretion in a T cell stimulation assay. The data showed that c7D3 has high binding affinity and excellent blocking bioactivity, supporting the further advancement for therapeutic application.

Acquired Immunodeficiency Syndrome ; epidemiology ; virology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Young Adult

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

BACKGROUND/OBJECTIVES: The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs. MATERIALS/METHODS: Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 microg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK. RESULTS: The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 microg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury. CONCLUSIONS: Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
Apoptosis ; Blotting, Western ; Centrifugation, Density Gradient ; Ficoll ; Flow Cytometry ; Glucose* ; Humans ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Protein Kinases ; Signal Transduction ; Stem Cells*

OBJECTIVETo investigate the potential preventive effects of metformin on non-alcoholic fatty liver disease (NAFLD) and roles of phospholipase A2/lysophosphatidylcholine pathway in hepatocyte lipoapoptosis in a rat NAFLD model induced by high-fat diet.

METHODMale SD rats (n = 36) were randomly divided into three groups with 12 rats in each and treated with different diet and drugs: group I: ordinary diet, group II: high-fat diet, group III: high-fat diet and metformin. Ten weeks later, the rats were sacrificed and their body weight and liver weight were obtained, serum lipid metabolic indexes, insulin resistance indexes and secretory phospholipase A2 (sPLA2), lysophosphatidylcholine (LPC) levels and other parameters were measured. Phospholipase A2 mRNA expression levels were measured by quantitative reverse transcription-polymerase chain reaction (RT-PCR). In addition, the histological changes of liver tissue were analyzed.

RESULTCompared to ordinary diet group, the rat's liver weight (g) (16.92 ± 2.49 vs. 12.16 ± 0.82), hepatic exponent (0.034 ± 0.004 vs. 0.026 ± 0.002), serum alanine aminotransferase (U/L) (45.43 ± 9.73 vs. 29.42 ± 6.73), triglyceride (mmol/L) (1.22 ± 0.24 vs. 0.85 ± 0.19), cholesterol (mmol/L) (2.00 ± 0.37 vs. 1.49 ± 0.33), lipoprotein(a) (mmol/L) (743.86 ± 32.19 vs. 648.42 ± 78.87), low-density lipoprotein (mmol/L) (1.31 ± 0.35 vs. 0.65 ± 0.22), insulin (mmol/L) (22.16 ± 5.16 vs. 16.86 ± 5.35), insulin resistance index(5.10 ± 1.45 vs. 3.59 ± 0.99), free fatty acid (mEq/L) (0.57 ± 0.10 vs. 0.35 ± 0.07), sPLA2 [µmol/(min·ml)] (0.130 ± 0.016 vs. 0.098 ± 0.024), lysophosphatidylcholine (µmol/L) (707.26 ± 92.48 vs. 508.87 ± 96.50), leptin (pg/ml (80.08 ± 17.73 vs. 65.11 ± 14.09), liver triglyceride (mg/g) (13.57 ± 0.65 vs. 12.03 ± 1.14), cholesterol (mg/g) (2.19 ± 0.15 vs. 1.94 ± 0.12) (P < 0.05) were significantly increased in high-fat diet group. Moreover, degree of hepatic steatosis was significantly higher and sPLA2 mRNA expression was also significantly increased. Secondly, in comparison with high-fat diet group, early metformin treatment significantly reduced the rat's body weight (g) (394.40 ± 33.10 vs. 491.86 ± 26.45), liver weight (g) (13.24 ± 1.16 vs. 16.92 ± 2.49), serum alanine aminotransferase (U/L) (30.40 ± 4.50 vs. 45.43 ± 9.73), triglyceride (mmol/L) (0.75 ± 0.19 vs. 1.22 ± 0.24), cholesterol (mmol/L) (1.61 ± 0.38 vs. 2.00 ± 0.37), insulin (mmol/L) (16.96 ± 5.60 vs. 22.16 ± 5.16), insulin resistance index (3.75 ± 1.41 vs. 5.10 ± 1.45), sPLA2 [µmol/(min·ml)] (0.101 ± 0.009 vs. 0.130 ± 0.016), lysophosphatidylcholine (µmol/L) (549.92 ± 90.78 vs. 707.26 ± 92.48), liver triglyceride (mg/g) (11.23 ± 1.70 vs. 13.57 ± 0.65), cholesterol (mg/g) (1.97 ± 0.20 vs. 2.19 ± 0.15) (P < 0.05). Moreover, degree of hepatic steatosis was significantly lower and sPLA2 mRNA expression was also significantly decreased by metformin. Thirdly, when compared to ordinary diet group, metformin could also significantly increase hepatic exponent (0.034 ± 0.004 vs. 0.026 ± 0.002) and low-density lipoprotein level (mmol/L) (0.96 ± 0.34 vs. 0.65 ± 0.22) (P < 0.05). However, it had no impact on hepatic steatosis and sPLA2 expression (P > 0.05).

CONCLUSIONIt was indicated that metformin has potent effects on improving lipid metabolism and insulin resistance in high-fat diet induced non-alcoholic fatty liver disease rat model. The liver protective mechanisms of metformin in non-alcoholic fatty liver disease may be contributed to down-regulation of secretory phospholipase A2 mRNA expression, decrease in serum secretory phospholipase A2, lysophosphatidylcholine, lower inflammatory response and protect mitochondrial function.

Animals ; Apoptosis ; Disease Models, Animal ; Down-Regulation ; Fatty Liver ; drug therapy ; enzymology ; pathology ; Insulin Resistance ; Lipid Metabolism ; Lysophosphatidylcholines ; metabolism ; Male ; Metformin ; pharmacology ; Non-alcoholic Fatty Liver Disease ; Phospholipases A2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction