Nonarteritic anterior ischemic optic neuropathy (NAION)is a common optic neuropathy seriously affecting the visual function in the middle-aged and elderly population.However,its pathogenesis is not completely clear,and therefore its treating efficacy is dissatisfactory.The current study on NAION is focused on the establishment of suitable animal model and the pathogenesis.In recent years,the relatively ideal animal models(including rodent and primate) have been established by photodynamic methods,which make people have more in-depth understanding on the pathophysiologic mechanism of NAION and lay the basis for the research of therapies.The selection of experimental animals,various induction methods and existing problems in the creation of NAION animal model were reviewed and analyzed in this artical.

ObjectiveTo observe the effect of early rehabilitation on poststroke anxiety and depression.Methods137 stroke patients with hemiplegia were divided into the rehabilitation group (70 cases) and control group (67 cases). All patients in both two groups were given routine clinical treatment, but the patients in the rehabilitation group were given regular early rehabilitation. All patients were evaluated with Bathel Index (BI), Fugl-Meyer Motor Scale (FMMS), Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) before and 3 months after treatment.ResultsAfter 3 months treatment, the scores of HAMD, HAMA, BI and FMMS of patients in the rehabilitation group increased significantly compared with those before treatment ( P<0.05～0.01), and those in the control group ( P<0.05). The scores of BI and FMMS of patients in the control group after treatment also increased significantly compared with those before treatment ( P<0.05). The incidences of depression and anxiety of the rehabilitation group were 22.86% and 5.71%, those of the control group were 40.30% and 16.42%, there was a significant difference between two groups( P<0.05).ConclusionThe early rehabilitation can obviously decrease anxiety and depression of stroke patients with hemiplegia.

Objective To explore whether arsenic trioxide(As2O3)-induced apopotosis in drug-resistant leukemia K562/ADM cells may induce in through endoplasmic reticulum stress leukemia cell apopotosis.Methods The apoptosis of K562/ADM cells was identified by double staining of FITC-Annexin V and propidium iodide(PI),the ultrastructure of the cells,endoplasmic reticulum and mitochondria were observed by transmission electron microscopy.Flow cytometry(FCM) was employed to assess mitochondrial inner membrane potential(??m),intracellular calcium concentration,cytochrome c(Cyt c) release and caspase-3 activity.The expression of GRP78 protein was analyzed by Western blot.Results During the apoptotic process of K562/ADM cells induced with 2 ?mol/L and 5 ?mol/L As2O3,the endoplasmic reticulum exhibited obvious expansion and degranulation,and the mitochondria illustrated inner and outer membranes fusion,reduced and confused cristae,swelling and vacuolization.The mitochondrial ??m decreased,the intracellular calcium concentration and releasing of cytochrome c from mitochondria increased,and caspase-3 was activated.Western blot result indicated upregulation of GRP78 protein at endoplas-mic reticulum in apopototic K562/ADM cells.Conclusion As2O3 can initiate the endoplasmic reticulum stress in K562/ADM cells,and induces to apoptosis of the drug-resistant cell via endoplasmic reticulum-mitochondrial pathway.

OBJECTIVETo evaluate in vitro effect of abnormal savda munziq (ASMq) on the proliferation and apoptosis of human hypertrophic scar fibroblasts (HSFs).

METHODSHSFs were divided into six groups to receive different treatments as group A (blank control group), group B-E (ASMq in different concentration), and group F(5-Fu). Each group contains six specimens. The HSFs were cultured in vitro. After culture for 48 hours, the CCK8 test and flow cytometry methods were used to detect the proliferation, cell cycle and apoptosis.

RESULTSThe proliferation of HSFs in the B, C, D and E groups was inhibited at G2/M period, while it was inhibited at G0/S period in group F (P < 0.05). The inhibition effect of ASMq (0.1-1.0 mg/ml) on the fibroblasts enhanced in a concentration-dependent manner. Flow cytometry analysis with annexin V-FITC and PI staining confirmed the apoptotic. When HSFs were exposed to ASMq at 1.0 mg/ml (group E) for 48 h, the percentage of apoptotic cells increased to (43.7 +/- 2.58)%, which was significantly higher than that of blank control group (2.2 +/- 0.59)%. The induced apoptosis effect was also increased in a concentration-dependent manner.

CONCLUSIONASMq has a inhibitory effect on the proliferation and an enhancement effect on the apoptosis of fibroblast. ASMq could be used as an effective drug for treatment of hypertrophic scar.

Apoptosis ; Cell Cycle ; drug effects ; physiology ; Cell Division ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cicatrix, Hypertrophic ; pathology ; Fibroblasts ; cytology ; drug effects ; Flow Cytometry ; Humans ; In Vitro Techniques ; Medicine, East Asian Traditional

ObjectiveTo investigate the effects of cannabinoid receptor 2 (cannabinoid receptor 2,CB2R) agonist JWHO15 on the hyperalgesia induced by remifentanil in a rat model of postoperative pain.Methods Sixty SD rats were randomly divided into 10 groups ( n =6 each ):control groups ( C1 and C2 ),incisional pain groups (I1 and I2),incisional pain plus JWHO15 groups (QI and FI),remifentanil groups (R1 and R2),and JWHO15 plus remifentanil groups ( QR and FR).Rats in group QL/QR and FI/FR were intrathecal injection with 10μg JWHO15 ( diluted in 10μl 20％ DMSO solution) and intraperitoneal administration with 100μg JWHO15 ( diluted in 10μl 4％ DMSO solution) respectively 30 min before plantar incision while rats in group C,I and R were received with the same volume of DMSO solution.Plantar incision surgery was operated in rats of group I,R,QI/FI,and QR/FR.In group R and QR/FR,remifentanil (0.04 mg/kg) was infused subcutaneously to rats with a pump for 30 min at the moment of surgical incision.The paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) at 24 h before incision and at 2 h,6 h,24 h and 48 h after incision were tested to evaluate the behavioral changes.ResultsCompared with group C and baseline,the level of PWMT and PWTL decreased at 2 h,6 h,24 h and 48h after incision in group Ⅰ (P＜ 0.01 ) ;Compared with group Ⅰ,the significant decrease of PWMT and PWTL were observed after incision in group R (P ＜ 0.05 ) ; Compared with group R,the significant increase of PWMT (7.78 ± 1.09) and PWTL ( 17.28 ± 1.58) were observed from 6 h after incision in group QR(P＜0.05).And the increase of PWMT (7.79 ±0.72,9.50 ± 1.17,7.86 ± 1.16) and PWTL ( 16.23 ± 1.50,19.53 ± 1.63,18.10 ± 0.93) were observed at 6 h,24 h and 48 h after incision in group FR(P＜0.05).ConclusionIntrathecal and intraperitoneal administration of JWHO15 in this investigation dose could relief remifentanil-induced hyperalgesia in a rat model of postoperative pain.

12E7 Antigen ; Antigens, CD ; metabolism ; Antigens, CD34 ; metabolism ; Cell Adhesion Molecules ; metabolism ; Diagnosis, Differential ; Head and Neck Neoplasms ; metabolism ; pathology ; Hemangioma ; pathology ; Humans ; Lipoma ; metabolism ; pathology ; Liposarcoma, Myxoid ; pathology ; Male ; Middle Aged ; S100 Proteins ; metabolism ; Soft Tissue Neoplasms ; metabolism ; pathology

Objective To investigate the effects of intrathecally cyclic AMP response element-binding protein(CREB) antisense oligodeoxynucleotide (ODN) on neuropathic pain behaviors.Methods Using mouse model of neuropathic pain induced by chronic constriction injury of sciatic nerve (CCI),24 male C57BL/6 mice successfully received intrathecal catheter implantation and without motor dysfunction were randomly divided into 4groups(n=6):Saline group(NS),CREB sense ODN group(S),CREB missense ODN group(M),CREB antisense ODN group(A).Mice in NS,S,M and A were intrathecally treated with Saline 5μ l,Sense ODN 5μg/5μl,Missense ODN 5μg/5μl and Antisense ODN 5μg/Sμl once daily on day 1 ～6 after CCI respectively.Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency(PWTL) were tested on day 1 before CCI and day 1,3,5,7,10,14,17,21 after CC(I).Results Mice in A group maintained the pain thresholds in the baseline and lasted at least 7 days after CCI ( 7 d,PWMT:( 0.81 ± 0.20 ) g vs ( 1.00 ± 0.19 ) g,P ＞ 0.05 ;PWTL:(5.96 ± 0.69) s vs (6.93 ± 1.08 ) s,P ＞ 0.05 ).The withdrawal thresholds in the ipsilateral hind paws of the mouse were significantly lower than baseline in A group on day 10 after CCI( 10 d,PWMT:(0.56 ±0.19)g vs (1.00±0.19)g,P＜0.05; PWTL:(3.93 ±0.28)s vs (6.93 ± 1.08)s,P＜0.05).Compared with NS group ( 10 d,PWMT:(0.56 ±0.19)g vs (0.37 ±0.08)g,P＜0.05; PWTL:(3.93 ±0.28)s vs (3.14 ±0.45)s,P＜0.05),S group,M group,the withdrawal thresholds of A group was significantly elevated on day 10 after CCI.These effects lasted up to at least day 21 after CCI.Conclusion Intrathecally treated with CREB antisense ODN in the development of neuropathic pain induced by CCI completely improved pain behaviors during the course of injection,and the effects of relief pain lasted at least 15d after no injection.

Objective To investigate the effects of repeated intrathecal cyclic AMP response elementbinding protein (CREB) antisense oligodeoxynucleotide (ODN) on the expression of NR2A in spinal cord in mice with neuropathic pain produced by chronic constrictive injury of the sciatic nerve (CCI).Methods Forty C57BL/6 male mice in which intrathecal catheter was successfully implanted were randomly divided into 4 groups ( n =10 each):normal saline group (group NS),CREB sense ODN group (group S),CREB missense ODN group (group M),and CREB antisense ODN group (group A).In groups NS,S,M and A,normal saline 5μl,sense ODN 5 μg/5 μl,missense ODN 5 μg/5 μl and antisense ODN 5 μg/5 μl were injected intrathecally once a day for 6 days,starting from the 1st day after CCI,respectively.Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured on day 1 before CCI and on day 1,3,5 and 7 after CCI.Five mice from each group were sacrificed on day 7 and 14 after CCI and the lumbar segment of the spinal cord (L3-5 )was removed for determination of NR2A expression using Western blot and RT-PCR.Results Compared with the baseline value,no significant change was found in PWMT and PWTL on day 1-7 after CCI in group A ( P ＞0.05),while PWMT and PWTL were significantly decreased on day 1-7 after CCI in groups NS,S and M (P ＜0.05).Compared with groups NS,S and M,the expression of NR2A mRNA and protein was significantly downregulated on day 7 and 14 after CCI in group A ( P ＜ 0.05).The expression of NR2A mRNA and protein was significantly up-regulated on day 14 after CCI compared with that on day 7 after CCI in all the groups.Conclusion Intrathecal CREB antisense ODN during the development of neuropathic pain can attenuate neuropathic pain and inhibition of the expression of NR2A in mouse spinal cord may be involved in the mechanism.

ObjectiveTo investigate the role of Akt/glycogen synthase kinase-3β (GSK-3β) signaling pathway in neuropathic pain in mice.MethodsThirty-six male C57BL/6 mice,aged 7-8 months,weighing 20-25 g,were randomly divided into 2 groups:sham operation group (group.S,n =9) and chronic constrictive injury (CCI) group (n =27).CCI was produced by placing loosely constrictive ligatures around the common sciatic nerve.Six animals were taken from each group and paw withdrawal threshold to mechanical stimulation (PWMT)and paw withdrawal latency to thermal stimuli (PWTL) were measured on day 1 before operation and on day 1,3,5,7,10,14,17 and 21 after CCI.Three mice were sacrificed on day 3 after CCI in group S and on day 1,3,5,7,10,14 and 21 after CCI in group CCI.The L3-5 segment of the spinal cord was removed for determination of the expression of Akt,phospho-Akt and phospho-GSK-3β by Western blot.Results Compared with group S,PWMT was significantly decreased and PWTL was significantly shortened on day 1-21 after CCI,the expression of Akt was significantly up-regulated on day 7-21 after CCI,and the expression of phospho-Akt and phospho-GSK-3βwas significantly up-regulated on day 1-21 after CCI in group CCI ( P ＜ 0.05).ConclusionAkt/GSK-3β signaling pathway is involved in the development and maintenance of neuropathic pain in mice.

Objective:To screen and characterize aptamers against BCR-ABL fusion protein.Methods:A 90bp single stranded DNA( ssDNA) random library was subjected to 13 rounds of selection against BCR-ABL fusion protein by systematic evolution of ligands by expotential enrichment ( SELEX ) method, the selected aptamers were cloned and sequenced.The primary sequences and structure of aptamers were analyzed by Clustal W and DNA Folding Sever and the percentage of the ssDNA pool bound to BCR-ABL core protein were determinated.Results: after 13 rounds selection, the percentage of ssDNA pool bound to BCR-ABL fusion protein increased from 0.3%to 47.1%,the results showed that affinities of the Aptamers were different,the second structure analysis revealed possible stem-loops for binding to BCR-ABL fusion protein,the affinity of aptamer A2 to BCR-ABL fusion protein was highest with Kd values as low as 72 nmol/L.Conclusion:Aptamers against BCR-ABL fusion protein has been identified by SELEX methods from a 90 bp single stranded DNA library.And provide certain reference for the clinical treatment of chronic myelogenous.