Neuropathic pain is a common chronic pain with complicated underlying mechanisms and difficult to treat, which badly disturbs the daily life of the patient and presents a significant burden to society by increasing healthcare resource utilization and costs. In the recent years, the pivotal role of glia-centered neuroinflammation and neuroimmunity in the development and maintenance of neuropathic pain has been recognized gradually. This review presents the current understanding of the role of glia in neuropathic pain and therapies of glia modulation.

To assess the clinical effect of HA regimen on newly diagnosed patients in chronic phase of chronic myeloid leukemia (CML). Ninety four cases of CML patients were grouped in accordance with the requirements on the basis of treatment regimens and Sokal risk index, and the clinical effects of HA regimen wer evaluated. We found that HA regimen showed satisfactory immediate effect on CML in chronic phase. CR rates achieved in high risk and medium risk groups(77 4%,20 0%) with HA were higher than that with Hu regimen(35 0%,0%). However, HA regimen was incapable of extending the duration of CML. So HA should not be used as first line treatment in the treatment on newly diagnosed patients in chronic phase of CML, except for high risk group whose symptoms could not be controlled with other regimens.

ObjectiveTo investigate the prevalence and distribution of 16S rRNA methylase gene and research the relationship with drug resistant spectrum.And preliminary explore its role in molecular epidemiology analysis.MethodsCollected 69 clinical isolates of non repetitive ESBL-producing Klebsiella pneumoniae in our hospital from Mar to Sep 2010.Detection 16S rRNA methylation enzyme gene by PCR,and analyze ESBL genetype and integron gene of the positive strains.All PCR products were sequenced for determination.Plasmid conjugation test and plasmid elimination method to determine dissemination of 16S rRNA methylase gene.Then we used ERIC-PCR genotyping technology for the establishment of DNA fingerprinting.ResultsIn sixty-nine strains,twenty isolates were rmtB positive (28.9％),two isolates were armA positive,and two strains coproduce rmtB and armA.All positive isolates carried the CTX-M gene,detemined by sequencing,14 strains of CTX-M-14 gene,6 strains of CTX-M-15 gene,14 strains carried TEM1 gene,8 strains carried SHY gene,sequencing showed that 5 strains of SHV-12 gene,3 strains of SHV-11 gene,3 strains carried OXA-10 gene,3 strains carried VBE-1 gene.In addition,the intl gene was found in 12 isolates of 20 rmtB positive strains.All the intl gene positive strains were divided into five kinds gene cassettes,which contained drfA25,drfA1,drfA12,aadA1,aadA2,sat and blaVEB-1 genes.Respectivily,16S rRNA methylase gene positive strains were divided into five genetypes using ERIC-PCR technology.A genetype was the advantage popular clones.Conjugative plasmid and elimination test found that rmtB gene was located in a plasmid in KP5 and KP16 isolates with A genetype,and can disseminate by conjugation.ConclusionA high prevalence of 16S rRNA methylase gene-rmtB was found among clinical ESBL-producing K.pneumoniae isolates in our hospital,which could lead to resistant to almost all aminoglycoside at a high level.Both horizontal gene transfer and clonal spread were responsible for the dissemination of the rmtB gene.In addition,K.pneumoniae co-producing ESBLs,16S rRNA methylation enzymes and class Ⅰ integron existed and were spreading.

Objective To study the effects of tyrosine kinase receptor B-brain-derived neurotrophic factor (TrkB-BDNF) signal pathway on the secretion of vascular endothelial growth factor (VEGF) and matrix metalloproteinases-9(MMP-9) of neuroblastoma.Methods We used all-trans retinoic acid (ATRA) to induce the high expression of TrkB in the SH-SY5Y cell line,and then added the ectogenid BDNF to activate the TrkB-BDNF and its three downstream signal pathways.TrkB-BDNF signal pathway was inhibited by specific tyrosine kinase inhibitor K252a.The three downstream signal pathway was respectively inhibited by LY294002 (the phosphatidylinositol 3-hydroxy kinase (PI3 K) pathway inhibitor)、U73122 (the phospholipase C pathway inhibitor) 、U0126(the mitogen activated protein kinase pathway inhibitor).Enzyme linked immunosorbent assay was used to detect the concentration of VEGF and MMP-9 protein in the SY5Y cell culture supernatants.Results VEGF [(485.89 ± 109.99) pg/ml] and MMP-9 [(15.73 ± 1.72) pg/ml] protein levels in neuroblastoma cells cultured in serum-free media in the group of ATRA + BDNF were significantly higher than that of the control group and ATRA alone group(P ＜0.05).VEGF [(272.42 ±86.33) pg/ml]and MMP-9 [(5.25 ± 1.44) pg/ml] protein levels in the group of ATRA + BDNF + K252a were significantly lower than those of the ATRA + BDNF group(P ＜ 0.05) and had no significant difference compared with the control group and the ATRA alone group(P ＞0.05).VEGF [(314.12 ±24.68) pg/ml] and MMP-9 [(4.91 ± 1.08) pg/ml] protein levels in the group of ATRA + BDNF + LY294002 were significantly lower than those of the ATRA + BDNF group(P ＜ 0.05) and had no significant difference compared with the control group and the ATRA alone group(P ＞0.05).VEGF [(444.08 ±64.49) pg/ml] and MMP-9 [(13.28 ±3.38) pg/ml] protein levels in neuroblastoma cells cultured in serum-free media in the group of ATRA +BDNF + U73122 had no significant difference compared with the ATRA + BDNF group(P ＞ 0.05).VEGF [(429.97 ± 19.95) pg/ml] and MMP-9 [(13.96 ± 4.45) pg/ml] protein levels in neuroblastoma cells cultured in serum-free media in the group of ATRA + BDNF + U0126 had no significant difference compared with the ATRA + BDNF group(P ＞ 0.05).Conclusion Activation of TrkB-BDNF signal pathway can increase the synthesis and secretion of VEGF and MMP-9 in human neuroblastoma cells.TrkB-BDNF signal pathway may be through activating its downstream PI3K pathway to increase the synthesis and secretion of VEGF and MMP-9 in human neuroblastoma cells.The synthesis and secretion of VEGF and MMP-9 can be inhibited by blocking the TrkB-BDNF signal pathway with K252a or blocking its downstream signal pathway PI3 K with LY294002.

Objective:To observe the development of tolerance and dependence to endomorphin 1(EM 1) and its regulation on ? opioid receptor(MOR) in rat brain,providing references for the mechanism of the EM 1 dependence. Methods: Totally 60 SD rats were randomly divided into saline, acute EM 1 treatment and chronic EM 1 treatment groups. For acute EM 1 treatment, rats were injected intracerebroventricularly with 10 ?g/kg EM 1 30 min prior to sacrifice. The chronic group were treated with EM 1 daily administration at 8:00 and 15:00 starting with 10 ?g/kg on day 1 to 50 ?g/kg on day 9. After chronic EM 1 treatment on day 1, 3, 6 and 9, the antinociceptive AD 50 or catatonic ED 50 values were determined by modified Dixon's method. The B max and K d values of 3H DAMGO saturation binding to MOR were measured by Scatchard analysis. The gene expression of MOR was appraised by RT PCR. Results:(1) EM 1 chronic treatment produced a high degree of tolerance to the antinociceptic and catatonic effects on the 3rd day (3.1 fold and 1.9 fold) and the 9th day (28.4 fold and 8.5 fold). The jumping times, weight lost and withdrawal score of rats were significantly higher than that of the control group after 9 d chronic EM 1 treatment. (2) After 9 d of administration with EM 1, the specific binding capacity and mRNA expression of MOR in rat cortex, midbrain and striatum were all decreased compared with those of the control and acute treatment groups, but the K d values were not significantly altered. Conclusion:Endomorphin 1 has the tolerant and dependent potent. For long term chronic treatment, Endomorphin 1 induces downregulation of the binding capacity and mRNA of MOR, which may be related to the dependence development.

Objective Beta platelet-derived growth factor receptor ( PDGFR-β)-mediated signaling plays a key role in mor-phine tolerance , but its molecular mechanisms are not yet completely understood .The present study aims to investigate whether the ex-tracellular signal-regulated kinase ( ERK) and cyclic AMP response element binding protein ( REB) signaling pathways are involved in the development of PDGFR-βactivation-induced morphine tolerance in rats . Methods Thirty-six adult male SD rats were randomly divided into six groups of equal number:normal saline (20μL), morphine (15μg), morphine +imatinib (morphine 15μg +ima-tinib 10μg), morphine +PDGF-BB (morphine 15μg +PDGF-BB 10 ng), imatinib (10μg), and PDGF-BB (10 ng), all treated intrathecally at 20μL once daily for 7 consecutive days .Paw withdrawal latency ( PWL ) was measured 1 d before and 30 min after medication at 1, 3, 5, and 7 days, respectively, followed by calculation of the maximal possible effect of analgesia (MPE).On the 8th day, PWL was again obtained from all the rats at 30 min after intrathecal injection of morphine (15μg).Then, all the animals were sacrificed and the L4-5 segment of the spinal cord was isolated for determination of the expressions of ERK , phosphorylated ERK ( p-ERK) , CREB, and phosphorylated CREB ( p-CREB) by Western blot. Results At 5 and 7 days after medication, MPE was significant decreased in the morphine group ([52.90 ±8.20] and [15.12 ±3.80] %) and the morphine +PDGF-BB group ([43.51 ±5.42] and [14.81 ±3.60] %) as compared with (100.00 ± 0.00) %in both groups at 1 day (P<0.05), but had no significant changes in the morphine +imatinib group at 1, 3, 5, and 7 days.After intrathecal injection of morphine on the 8th day, MPE was (16.22 ±2.51) %in the morphine group, (15.22 ±3.50) %in the morphine +PDGF-BB group, and (35.21 ±4.51) %in the PDGF-BB group, all remarkably lower than (100.00 ±0.00) %in the control group (P<0.05).There were no significant differences in the expression levels of ERK and CREB among the six groups.The expressions of spinal p-ERK and p-CREB were markedly increased in the morphine , morphine +PDGF-BB, and PDGF-BB groups as compared with the control group (P<0.05), but significantly decreased in the morphine +imatinib group in compari-son with the morphine group, (P<0.05). Conclusion The PDGFR-βsignaling pathway plays an important role in the develop-ment of tolerance to morphine-induced analgesia and its underlying mechanisms may be associated with the activation of the ERK and CREB pathways .

Objective:To prepare poly-L-lactic acid(PLLA)electrospun nanofibers carrying icariin(ICA)(ICA /PLLA)and to evaluate the effects of the ICA /PLLA on MC3T3-E1 cells.Methods:ICA solution was dispersed into PLLA solution,and electrospun fibers were fabricated by W/O emulsion method.The morphology of ICA /PLLA was observed by SEM.The in vitro release kinetics of ICA /PLLA was examined.The attachment of MC3T3-E1 cells on ICA /PLLA was examined by propidiumiodide(PI)labling and ob-served under fluorescent microscope.The proliferation of the cells was measured by MTT assay.The differentiation of the cells was ob-served by alkaline phosphatase (ALP)assay.Results:In vitro,ICA was effectively released from ICA /PLLA for 22 days,cells were attached well on the surface in all groups,ICA did not affect the proliferation of MC3T3-E1 cells(P >0.05),but increased the ALP activity(P <0.05)of the cells.Conclusion:ICA /PLLA can effectively control the release of ICA and promote the differentiation of MC3T3-E1 cells.

Objective: To investigate the analgesic effect and impact of lornoxicam on the expression of plasma IL-6 and IL-10 in patients undergoing upper abdominal surgery.Methods:Sixty patients undergoing upper abdominal surgery were randomly allocated into three groups,morphine group(M,n=20),postoperative lornoxicam group(L,n=20) and preemptive lornoxicam group(P,n=20).For group M the subjects received patient controlled intravenous analgesia(PCIA) with morphine(loading dose 0.05 mg/kg,bolus 1 mg,lockout time 10 min,background dose 0 mg) after the surgery.While in group L,8 mg lornoxiam was administered at the end of the surgery,then the same morphine PCIA scheme as in group M was used in combination with intermittent intravenous lornoxiam(8 mg per injection) at 12,24 and 36 h after the surgery.Except that the first 8 mg lornoxicam was injected 30 min before the operation,the analgesic paradigm of group P was similar to group L.The analgesic effect assessed by VAS at rest,the consumed dosage of morphine,and the adverse effects as nausea and vomiting,were recorded at 4,8,12,24 and 48 h.Furthermore,2 ml of the venous blood was drawn before the induction of anesthesia 2,6,12,and 24 h after the surgery to measure the levels of interleukin 6(IL-6) and interleukin 10(IL-10).Results: During the 48 h observation,the VAS at rest was not statistically significant in the three groups,but more morphine was consumed in group M than in group L and group P.There was no difference among the three groups in the incidence of such adverse effects as nausea or vomiting.The basic levels of IL-6 and IL-10 were too low to be measured.The concentrations of IL-10 and IL-6 reached the peak at 2 and 6 h after surgery respectively,and the level of IL-10 in group M was significantly lower than in groups L and P at 2 h.In contrast,the level of IL-6 in group M was significantly higher than in group L and group P at 6 h,and even higher than in group P at 12 h. Conclusion: Lornoxicam,especially when administered before upper abdominal operation,could significantly decrease the dose of morphine for postoperative analgesia and attenuate the inflammatory cytokine response after surgery.

Objective: To investigate a moderate dose of levobupivacaine in spinal anesthesia for caesarean section.Methods: Eighty parturients undergoing caesarean section were randomly divided into 4 groups: GroupⅠ(0.75% levobupivacaine 1.00ml+10% glucose 1.00ml+cerebrospinal fluid 1.00ml),GroupⅡ(0.75% levobupivacaine 1.33ml+10% glucose 1.00ml+ cerebrospinal fluid 0.67ml),Group Ⅲ(0.75% levobupivacaine 1.67ml+10% glucose 1.00ml+ cerebrospinal fluid 0.33ml) and Group Ⅳ(0.75% levobupivacaine 2.00ml+10% glucose 1.00ml).The spinal puncture sites were all located at L_2,3.The onset time of sensation block,the highest plane of analgesia,the time to reach the highest plane of analgesia,the time of regression to the L_1 segment,the degree of motor block,VAS scores,the degree of muscle relaxation,the rate of hypotension incidents and neonatal Apgar scores were recorded. Results: There were no statistically significant differences in the onset time of sensation block,the time to reach the highest plane of analgesia and the highest plane of analgesia among the 4 groups.But the durations of regression to the L_1 segment were dramatically shorter in GroupⅠand Ⅱthan in Group Ⅲ and Ⅳ(P

Objective: Little has been reported on the utilization of the preoperative preparing room before anesthesia.This article aimed to investigate how to improve work efficiency in the operation theatre by utilizing the preoperative preparing room.Methods: Two hundred patients undergoing elective surgery were equally randomized into an operation room group and a preoperative preparing room group,for which the preoperative preparations were made in the operation room and the preoperative preparing room,respectively.Records were made of such parameters as the anxiety score,mean arterial pressure(MAP) and heart rate(HR) of the patients,as well as the surgery rotation time.Results: The anxiety score,MAP and HR were significantly lower(P