Breast cancer is a heterogeneous disease.Its invasion and metastasis,recurrence and part of the chemotherapy drug tolerance are currentlv difficulties of treatment.Breast cancer stem cells have the ability of selfrenewal,proliferation and differentiation potential,which may correlate closely with breast cancer recurrence,treatment failure.This assay aims to briefly analyse markers and significance of breast cancer stem cells,and the relationship between the treatment of breast cancer and breast cancer stem cells.

Objective To analyze the effect of implementing traditional Chinese medicine (TCM) clinical pathway on family sickbed patients.Methods Those family sickbed patients with herpes zoster or facial neuritis were involved in this study.Their medical records and data of ‘Family sickbed quality control scale’ were collected,in which there are methods of TCM clinical pathway,decoction of the Chinese Medicine,ingredients and treatment procedures of the topically used TCMs,and acupuncture treatment procedures were documented.The family sickbed days,prognosis,informed rate and satisfaction rate were analyzed before and after TCM clinical pathway treatment.Results In the treatment group,the family sickbed days (11.67± 1.91)d and referral rate 12.20％ (10/82) were significantly lower (P＜ 0.01) than those in the control group [(1 3.88 ± 2.61) d,50.00％ (41/82) respectively].The rate of cure87.80％ (72/82),the rate of informed patient 97.56％ (80/82) and the rate of satisfaction91.46％ (75/82) were significantly higher(P＜ 0.01)than those in the control group [50.00％ (41/82)、65.85％ (54/82)、50.00％ (41/82) respectively].Conclusion The clinical pathways for family sickbed patients with herpes zoster or facial neuritis were effective.

0.05).Left ventricular mass index and the apoptotic rate of cardiac muscle cells were decreased in low-and high-dose herbal medicine groups(P

Objective To investigate the effect of propofol exposure on neuroapoptosis in pri-mary cultured cortical neurons and its mechanisms.Methods Cortical neurons were primarily cultured for seven days,then divided into two groups:control group (treated with equal volume of 20% in-tralipid),propofol-treated group (treated with 500 μmol/L propofol).The neurons were treated for 12 h.The neuron viability was determined by MTT.Neuroapoptosis was identified by Hoechest 33 258 dying.Mitochondrial membrane potential was measured by the fluorescent dye rhodamine 123 (Rh123).Western blot was performed to detect the level of cyt-c and cleaved-caspase-3.Results Neu-rons survival rate (54.4%±6.4%)in the propofol group was significantly lower than that of control group (99.8% ± 4.1%) (P < 0.05 ), the rate of neuronal apoptosis (46.5% ± 5.3%) was significantly higher than that of control group (7.2%±0.9%)(P <0.05),mitochondrial membrane potential (59.6%±4.3%)was significantly lower than that of the control group (99.9% ± 5.7%) (P <0.05 ),cyt-C protein level (0.38 ± 0.03 )was significantly higher than that of control group (0.1 5±0.02)(P < 0.05 ),level of cleaved-caspase-3 protein level (0.46 ± 0.04)was significantly higher than that of control group (0.13±0.02)(P <0.05).Conclusion Propofol induces neuroapo-tosis in primary cultured cortical neurons,which is associated with the decreased level of MPP and the increase levels of cyt-c and cleaved-caspase-3.

To investigate the effects of Tianqi Pingchan (TQPC) Granule, a compound traditional Chinese herbal medicine with antitremor activity, on levodopa-induced dyskinesia and the expression of G protein-coupled receptor kinase 6 (GRK6) in rats with Parkinson disease (PD).

Objective To investigate the relationship between G protein-coupled receptor kinase 6 (GRK6) and N-methyl-D-aspartate (NMDA) receptor in the mechanism study underlying motor complications in Parkinson's disease (PD).Methods The rat models (n= 25) of Parkinsonism related motor complications were established and were randomly divided into levodopa-induced dyskinesia (LID) group (n= 10,intraperitoneal injection of levodopa for 23 d),MK-801 treatment group (n= 10,intraperitoneal injection of MK-801 at day23 after intraperitoneal injection with levodopa for 22 days) and PD group (n= 5,intraperitoneal injection of vitamin C).Another 5 rats were served as controls (sham-operation group).The behavior changes of rats in MK-801 treatment group were observed,and the expression of GRK6 in the striate of rats was detected by immunohistochemistry and Western blot.Results After the chronic treatment with levodopa methyl ester,PD rats displayed abnormal involuntary movements,which was similar to levodopainduced dyskinesia in PD patients.Immunohistochemistry showed that GRK6-positive cells of lesion side were decreased in LID rats as compared with PD rats [(3.23±0.41 ) × 103 vs.(4.81 ± 1.31 ) ×103,P＜0.01].Rats in MK-801 treatment group displayed the decreased AIM scores and increased peak rotation,and the increased GRK6-positive cells of lesion side as compared with LID rats (P＜0.05).Western blot showed that the levels of GRK6 was 83.7% ±2.1% in PD group (presented as lesion side/unlesion side),76.8% ± 2.2% in LID group and 91.1% ± 2.7% in MK-801 treatment group (intergroups comparison:all P＜0.05).These results were in accordance with the results of immunohistochemistry.Conclusions Antagonist of NMDA receptor can be used to reduce the motor complications in rats.It may be due to increased GRK6 which inhibits the overactivation of glutamic acid receptors.

Objective To investigate the effect of BML-111 (the analogue of lipoxin) on uterine Hela cell (cervix cancer cell line) proliferation and the underlying mechanism. Methods Hela cells were stimulated by 50, 100, 200 and 400 μg/L BML-111, respectively, and cell viability was determined by MTT assay. Hela cells were divided into three groups:the control group (no treatment), the BML-111(200μg/L) group and the BML-111(200μg/L)plus Boc-2 (10μmol/L)group. Expression and location of P53 protein were detected by immunofluorescence. Expressions of NF-κB p65,P53 and CyclinD1 protein were detected by Western blotting. Results BML-111 (100, 200 and 400 μg/L) could effectively inhibit Hela cell viability compared with the control group (P < 0.05). P53 expression was shown decreased in both the nucleus and the cytoplasm without any change of P53 location , however, Boc-2 could reverse this effect. BML-111 could effectively inhibit P53 and CyclinD1 expression via NF-κB pathway and the effects could also be inhibited by Boc-2. Conclusions BML-111 can effectively inhibit Hela cell proliferation via FPR2 and NF-κB pathway.

To investigate the neuroprotective of ligustilide (LIG) against glutamate-induced apoptosis of PC12 cells, cell viability were examined by MTT assay. Flow cytometry was applied to assay cell apoptosis rate. Intracellular calcium concentration was measured by using fluorescent dye Fluo-3/AM. Cytochrome C (Cyt C), Caspase-3, Bax and Bcl-2 protein expression were assayed by western blot. The results showed that glutamate is cytotoxic with an inhibitory concentration 50 (ID50) of 15 mmol · L(-1). Pretreatment with LIG (1, 5, 15 μmol · L(-1)) significantly improved cell viability. The apoptosis rate in glutamate-induced PC12 cells was 13.39%, and decreased in the presence of LIG (1, 5, 15 μmol · L(-1)) by 9.06%, 6.48%, 3.82%, separately. Extracellular accumulation of Ca2+ induced by glutamate were significantly reduced by LIG. The results of western blot manifested that pretreatment LIG could decrease the release of Cyt C from mitochondria, down-regulate Caspase-3 protein expression and up-regulate Bcl-2/Bax ratio, thereby protects PC12 cells from apoptosis. In summary, LIG had protective effect on glutamate-induced apoptosis in PC12 cells through attenuating the increase in intracellular Ca2+ concentration, and inhibiting the release of Cyt C from mitochondria to cytoplasm.

ObjectiveTo investigate the effect of MK-801 on levodopa-induced dyskinesia (LID)in Parkinson' s disease (PD). MethodsRat models ( n = 25) of Parkinsonism related motor complications were established and were randomly divided into levodopa-induced dyskinesia (LID) group (n = 10), MK801 treatment group (n = 10) and PD group (n =5). Another 5 rats were served as control group. The behaviors of LID rats treated with MK-801 were observed. Immunohistochemistry and Western blot analysis were used to determine the expression of β-arrestin1 in the striate of rats.Results After MK-801 treatment, abnormalinvoluntarymovementscores and peakturning weredecreasedin LIDrats.Immunohistochemistry showed that β-arrestin1-positive cells of the lesioned side ((2. 95 ± 0. 44) × 104) in LID rats were decreased compared to the contralateral side ( ( 3.78 ± 0. 37 ) × 104, t = 5. 415, P ＜ 0. 05 ).Western blot showed that the levels of β-arrestinl in PD group ( presented as lesioned side/contralateral side) were ( 81.02％ ± 2. 23％ ). The levels of β-arrestin1 (64. 88％ ± 3. 10％ ) were deceased in LID rats compared to PD rats ( t = 9.47, P ＜ 0. 01 ). However, the levels of β-arrestin1 ( 89. 26％ ± 1.90％ )were increased in MK-801-treated rats (t = 14. 82, P ＜0. 01). ConclusionsMK-801 reduces LID in PD rats. The beneficial effect of MK-801 may be mediated through the increased expression of β-arrestinl which in turninhibits the overactivation of glutamate receptors.

Objective To evaluate the effect of dexmedetomidine on the expression of c-fos protein in the dorsal root ganglion neurons in a rat model of neuropathic pain (NP).Methods Seventy-two adult male SpragueDawley rats,weighing 180-240 g,were randomly divided into 3 groups (n =24 each) using a random number table:sham operation group (group S),group NP,and dexmedetomidine group (group Dex).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 350 mg/kg.The right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread in NP and Dex groups.In group Dex,dexmedetomidine 50μg/kg was injected intraperitoneally once a day starting from the end of operation until the animals were sacrificed.The equal volume of normal saline was given instead of dexmedetomidine in S and NP groups.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before ligation (T0,baseline) and 3,7 and 14 days after ligation (T1-3).Eight animals were sacrificed after measurement of pain threshold at T13 and the dorsal root ganglions of the lumbar segments (L44) were removed for detection of c-fos expression (by immuno-histochemistry).Results Compared with group S,MWT was significantly decreased,TWL was shortened,and the expression of c-fos protein was up-regulated at T1-3 in NP and Dex groups.Compared with NP group,MWT was significantly increased,TWL was prolonged,and the expression of c-fos protein was down-regulated at T1-3 in Dex group.Conclusion Dexmedetomidine can inhibit upregulation of c-fos protein expression,thus attenuating NP in rats.