It is now widely accepted that platelet aggregation plays an important role in physiological hemostasis and pathological thrombosis associated with cardiovascular and cerebrovascular diseases. Anti-platelet aggregation drug research is also a hot spot of current research. The biggest challenge of antiplatelet therapy has been the molecular overlap of the hemostasis and thrombosis, leading to a serious risk of bleeding. Recent studies have emphasized the importance of shear stress generated from blood flow, which will primarily drive platelet activation and aggregation in thrombosis. So if we can take advantage of the differences between the physiological and pathological vascular blood flow environment, the development of selective anti-platelet therapy may be a safer treatment for cardiovascular and cerebrovascular diseases. In this review, we discuss the underlying mechanisms of shear-induced platelet activation. Later, we summarize the effects and mechanisms of compounds and traditional Chinese medicine on shear-induced platelet activation. The aim is to provide a reference for the study of biological pharmacology of traditional Chinese medicine for promoting blood circulation and removing blood stasis.

Objective To investigate the efficacy and safety of low-dose prednisone combined with methotrexate (MTX) and hydroxychloroquine (HCQ) in the treatment of rheumatoid arthritis (RA).Methods In this 12-week study,150 patients with active rheumatoid arthritis were randomly divided into two groups:prednisone group (70 cases who were received prednisone 5 ～ 10 mg/d + MTX 10 mg/w +HCQ 0.2 g/d) and control group (80 cases who were treated by Meloxicam 7.5 mg/d + MTX 10 mg/w +Leflunomide (LEF) 20 mg/d).The primary end-points were tender and swollen joint counts,visual analogue scales (VAS),and global physician and patients assessments of disease.The secondary end-points were morning stiffness time,C-reactive protein,erythrocyte sedimentation rate,the Health Assessment Questionnaire (HAQ),DAS28 and ACR20,ACR50.Results After 12 weeks,in terms of primary endpoints,tender and swollen joint counts,VAS and global physician assessments in the prednisone group were improved significantly [(4.5 ± 2.5),(3.2 ± 3.36),(21 ± 15),(24.2 ± 16.4),(20.2 ± 10.4) vs (6.4 ±5.84),(6.6±5.5),(46±14),(37.9±19.7),(34.1±12.4),P ＜0.05orP ＜0.01].In terms of secondary end-points,the prednisone group produced higher response rates [HAQ score (0.93 ± 0.52),CRP(10.2 ± 5.8) mg/L,ESR(30 ± 14) mm/h,morning stiffness time (32.0 ± 32.3) min,DAS 28 score (3.1±0.9) vs (1.22 ±0.81),(16.3±10.1)mg/L,(33±29)mm/h,(54.7±45.4)min,(4.9±1.9),P ＜0.05 orP ＜0.01].The incidence of adverse events was similar between two groups (43％ vs 49％,P ＞ 0.05).Conclusions Low-dose prednisone combined with MTX and HCQ produced rapid and relevant improvements in RA signs and symptoms.

Objective:To establish the median databases of serum markers for Down's syndrome screening during the second trimester of pregnancy women in the north-central area of Jiangxi Province.Methods:Time-resolved fluorometry was used to detect the serum contents of AFP free β-hCG and uE3 in 57 548 pregnant women during 15-20 gestational weeks.Risk evaluation was conducted by LifeCycle 4.0.SAS 9.2 software was used to establish a model of the median fitted equation.The newly constructed median system was used to reassess the risk of Down's syndrome development in pregnant women.Results:The medianand built in medianof north-central region in Jiangxi Province are significantly different (Z=2.201,P=0.028).The relationship between the median of the triple index and the gestational age was analyzed by the weight regression model.The relationship between the MoM value and the weight was used to calculate the reciprocal model.The median of the new system was more efficiency than the built in median.In the median of the new system than the reference,the detection rate improved from 62.75％ to 72.55％,false positive rate reduced by 5.84％ to 4.94％.Conclusion:The newly constructed median system is suitable for Down's syndrome screening in the north-central region of Jiangxi Province.

Aim To investigate the effect of phenyle-thanol glycosides from Cistanche tubulosa(CPhGs) on the proliferation and activation of rrPDGF-BB induced HSC and their target points for resisting hepatic fibro-sis,to elucidate the molecular mechanism in molecular level, and provide basic data for the further develop-ment of new drugs. Methods HSCs were cultivated by CPhGs with different concentrations ( 0 , 3. 91 , 7. 81 , 15. 63 , 31. 25 , 62. 50 , 125. 00 , 250. 00 , and 500 mg ·L-1 ) and IC50 of CPhGs was determined. CPhGs with different concentrations ( 25 , 50 , 75 , 100 mg · L-1 ) were selected, and after the cells were stimulated with rrPDGF-BB, cell proliferation was determined by MTT. ERK1/2 ,α-SMA, c-fos, c-jun and Collagen I mRNA and Erk1/2 ,P-Erk1/2 and CollagenⅠprotein ex-pressions were assayed by RT-PCR and Western blot. Results CPhGs of ( 50 ~100 ) mg · L-1 concentra-tions groups could effectively inhibit rrPDGF-BB-medi-ated proliferation(P<0. 05) and CPhGs of(25~100) mg·L-1 concentrations groups had no significant cyto-toxicity( P >0. 05 ) . CPhGs of ( 25 ~100 ) mg · L-1 concentrations groups could inhibit ERK1/2 ,α-SMA,c-fos, c-jun and CollagenⅠmRNA levels, and also ob-viously inhibited Erk1/2 ,P-Erk1/2 and Collagen Ⅰ pro-tein expression on HSC. Conclusions CPhGs has the protective effect against hepatic fibrosis. The mecha-nism of this process may involve the interference with PDGF/ERK1/2 signaling pathway and inhibiting the activation and proliferation of HSC.

OBJECTIVE To study the anti-fibrotic effect of Cistanche phenylethanoid glycosides (CPhG) in bovine serum albumin (BSA)-induced liver fibrosis in rats and its possible mechanism METHODS Seventy-five SD rats were randomly divided into six groups:normal control(distilled water-treated),model(BSA-treated),positive drug〔BSA-treated+compound Biejiarangan tablets(BJRG) 0.6 g·kg-1〕,and BSA-treated+CPhG(0.125,0.25 and 0.5 g·kg-1)groups. There were thirteen rats in each BSA-treated+CPhG(0.125,0.25 and 0.5 g·kg-1)group and twelve rats in other groups. Subcutaneous injection and tail vein injection of BSA immunity were used to induce the rat liver fibrosis model. Meanwhile, different therapeutic drugs were ig adminstered to rats. After the experimental period,rats were fasted for 12 h prior to 10%chloral hydrate administration and immediately euthanized. The liver was weighed to calculate the liver index. Glutamic-pyruvic transaminase (GPT),glutamic-oxalactic transaminase (GOT),alkaline phosphatase(ALP),total protein(TP)and albumin(ALB)were evaluated by the Mind-Ray automatic biochemical analyzer. The density of hydroxyproline (HyP) in liver tissues was determined using a spectrophotometric method according to the kit′s instructions. Histopathological changes and expressions of typeⅠ and typeⅢcollagens in liver tissues were also determined by immunohisto?chemical staining. RESULTS Compared with the normal control group,collagen fibers of liver tissues in the model group extended their links and enveloped the entire lobule,causing lobular structural damage and the formation of pseudolobules. The liver index(P<0.05),GPT,GOT,ALP,TP and ALB serum levels(P<0.05),HyP content(P<0.01)were significantly increased,so was the expression of typeⅠcollagens and typeⅢcollagens(P<0.01)in the model group. Compared with model group,various doses (0.125,0.25 and 0.5 g · kg-1) of CPhG significantly reduced the BSA-induced elevation of the liver index;GPT,GOT,ALP,TP and ALB serum levels(P<0.05),and HyP content decreased(P<0.01);the morphology of the pathological tissue sections was close to that of the normal control group,and CPhG significantly reduced the expression of two types of collagens(P<0.01). CONCLUSION CPhG can significantly reduce the degree of BSA-induced liver fibrosis in rats. The mechanism may be associated with down-regulation of two types of collagens and suppression of the activation of hepatic stellate cells.

Objective To isolate and culture sweat gland epithelial cells in vitro,and to study the effects of acetylcholine (ACh) on intracellular flee calcium concentration ([Ca~(2+)]i) of cultured sweat gland epithelial cells.Methods Sweat glands epithelial cells were collected by enzymatic digestion.After ACh was added to the primary and first passage cells,[Ca~(2+)]i was examined using confocal laser scanning microscopy (CLSM) and the Ca~(2+) sensitive dye Fura 3/AM.Results The primary and first passage epithe- lial cells grew well.After ACh was added,opening of the calcium channel and significant [Ca~(2+)]i increase were observed when the primary and first passage cells were incubated with high concentration of calcium (2 mmol/L);no significant [Ca~(2+)]i increase was observed in those cultured without calcium.Conclusion Upon stimulation with ACh,calcium channels of cultured primary and first passage sweat gland epithelial cells would open,influx of extracellular Ca~(2+) occurred,which resulted in an increase of [Ca~(2+)]i.Extracellular bound calcium was therefore converted into intracellular free calcium.

In temporomandibular disorders (TMD), pain takes place when neuropeptides stimulate synovial tissue to produce several cytokines such as interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, which activate neurons and glia of synovial membrane at the bilaminar regions of temporomandibular joint (TMJ). It has been reported that, after neurogenic differentiation, the synovial mesenchymal stem cells (SMSCs), deriving from TMJ, possess the same cytological features as the neuronal cells. This study examined the ability of substance P (SP) and calcitonin gene-related peptide (CGRP) to stimulate SMSCs and neurogenic SMSCs secreting inflammatory cytokines during TMD, evaluated the mutual effects of inflammatory cytokines and neuropeptides and tested the analgesic effect of hyaluronic acid (HA). The levels of IL-1β, IL-6 and TNF-α in SMSCs and neurogenic SMSCs in the presence of neuropeptides were measured by ELISA. SP and CGRP produced by SMSCs and neurogenic SMSCs were determined by RT-PCR and Western blotting. The results showed that the expression of SP and CGRP was significantly enhanced in the neurogenic SMSCs in response to IL-1β, IL-6 and TNF-α, and the effect was remarkably inhibited by HA. IL-1β, IL-6 and TNF-α, in return, could be enhanced in the neurogenic SMSCs upon stimulation by SP and CGRP. Neuropeptides and inflammatory cytokines might work mutually on the TMD pain. The HA-mediated analgesic effect may be implicated in the inhibition of SP and CGRP expression in neurogenic SMSCs.

Objective: To investigate the effect and mechanism of helix B surface peptide (HBSP) on myocardial ischemia reperfusion injury (MIRI) in experimental mice.
Methods: The MIRI model was established by ligation of anterior descending coronary artery of the mice for 45 min and followed by corresponding treatment at 5 min before reperfusion. A total of 64 male ICR mice were randomly assigned to 4 group:①Sham group,②MIRI group, the mice received normal saline at 5 min before reperfusion,③HBSP group, MIRI mice received HBSP at 5 min before reperfusion and④HBSP+PD98059 group, MIRI mice received PD98059 (a speciifc blocker of ERK1/2) at 20 min before reperfusion and followed by HBSP at 5 min before reperfusion.n=16 in each group, all animals were treated for 2 hours. The area of myocardial infarction (MI) was detected by TTC-EB double staining method, the myocardial apoptosis rate was examined by TUNEL method, the levels of protein expression of ERK1/2 and phosphorylation of ERK1/2 were measured by Western blot analysis.
Results: Compared with MIRI group, HBSP group presented decreased MI area, decreased myocardial apoptosis rate and increased phopsphorylation level of ERK1/2, allP<0.05. Compared with HBSP group, HBSP+PD98059 group showed decreased phopsphorylation level of ERK1/2, increased myocardial apoptosis rate and increased MI area, allP<0.05.
Conclusion: HBSP may reduce the MI area via inhibiting myocardial apoptosis and therefore, protecting the experimental mice from MIRI; the mechanism might be related to the activation of ERK1/2 pathway.

OBJECTIVETo search for an effective method for treatment of prolapse of lumbar intervertebral disc.

METHODSNinety-four cases were randomly divided into a treatment group of 48 cases and a control group of 46 cases. The treatment group were treated by acupuncture and moxibustion combined with sacral injection and the control group with simple sacral injection. Their therapeutic effects were compared.

RESULTSThe cured and total effective rates were 64.6% and 97.9% in the treatment group, and 37.0% and 89.1% in the control group, with statistically significant differences between the two groups (both P < 0.05).

CONCLUSIONAcupuncture and moxibustion combined with sacral injection has a significant therapeutic effect on prolapse of lumbar intervertebral disc.

The aim of this research is to refine the protocol of purification of SA and identify the character of SA. By utilizing the cold-denaturing method, most of other kinds of protein were screened out and SA was purified from the fermentation broth of L-183 by using the refined affinity chromatography method. The rate of recollection was checked to be 75%～85%. By identification, it is indicated that the molecular weight of self-made SA was 74.5kD, the biotin-combining number 3.2, the activity 11.2u/mg, the pI around 7.4. So, the essential characters of SA are same as described by documents.