Table of Content

    05 August 2015, Volume 35 Issue 8
    Mutation analysis of the pathogenic gene in a Chinese family with G6PD deficiency
    2015, 35(8):  1011-1014. 
    Asbtract ( 965 )   PDF (813KB) ( 543 )  
    Related Articles | Metrics
    Objective In order to recognize the underlying mutation site as well as its inheritance model, all the thirteen exons of G6PD gene were sequenced for a family trio with G6PD deficiency. Methods We collected the family trio with G6PD deficiency in Huizhou of Guangdong Province, a region of high prevalence of G6PD deficiency. The family trio includes the proband, his affected mother and healthy father.Their blood samples were collected and genomic DNA were extracted. Sequence analysis was performed in thirteen exons by PCR and DNA sequencing. Results The results indicated that the proband and his mother shared an identical mutation (c.95A>G, p.His32Arg) in exon 2 of G6PD gene. This mutation causes histidine to be replaced with arginine (CAC>CGC). However, no single mutation was found in his father. Three bioinformatics tools predicted that this mutation is detrimental to the function(s) of its associated protein. Conclusions The mutation, c.95A>G, following an X-linked dominant inheritance model, is a causal site for G6PD deficiency.
    Increased expression of MKP-1 and reduced production of NO in brain of rats after traumatic injury
    2015, 35(8):  1015-1019. 
    Asbtract ( 521 )   PDF (892KB) ( 442 )  
    Related Articles | Metrics
    Objective To detect expressive changes of MKP-1 and measure NO content in the rats of pericontusional cerebral cortex after traumatic brain injury (TBI), discuss regulatory role and molecular mechanism of MKP-1 on NO generation after TBI. Methods We constructed TBI model by the Feeney's method. Nitric oxide detection kits were used to measure NO content in pericontusional cerebral cortex between control group and TBI group. Distribution of MKP-1 was detected by immunohistochemistry. Western blot analysis were performed to detect expression level of MKP-1, endothelial NOS and MAPKs in the rats of pericontusional cerebral cortex after TBI. Result NO level significantly decreased at 3h、6h、24h and 72h with concentration as 20.8 ± 2.5 μmol/L 、23.9 ± 3.8 μmol/L 、24.0 ± 1.6 μmol/L 、26.8 ± 2.6 μmol/L (P<0.05) respectively, compared with the control as 34.4 ± 3.2 μmol/L after TBI. The positive staining MKP-1 cells were scattered distributed in pericontusional cerebral cortex with brown cytoplasma and processes and increased significantly at 3h and 6h after TBI. Compared to the control group, the protein expressions of MKP-1 were increased at 3h and 6h respectively with normal level at 24h after TBI(P<0.05). While the protein levels of eNOS were decreased at 3h and 6h respectively after TBI (P<0.05). The protein expressions of pERK and p-p38 were both decreased at 3h and 6h respectively after TBI compared with control group (P<0.05).Conclusion Increased MKP-1 expression in pericontusional cerebral cortex after TBI specifically decreased the expression level of pERK and p-p38 MAPK with the pJNK intact to down-regulated the expression of endothelial NOS, which decreased NO content attributed to the defect of cerebral blood flow.
    The effect of Vaspin on TNF-α-induced NF-κB and PI3K/Akt signaling pathways in HUVEC
    2015, 35(8):  1020-1024. 
    Asbtract ( 608 )   PDF (760KB) ( 508 )  
    Related Articles | Metrics
    Objective To investigate the effects of visceral adipose tissue-derived serpin (Vaspin) on nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3-kinase(PI3K)/Akt signal pathways in human umbilical vein endothelial cells (HUVEC) stimulated by tumor necrosis factor-α (TNF-α) to elucidate the role of Vaspin in human endothelial cells of inflammation and insulin resistance. Methods HUVEC were isolated and cultured in vitro. A NF-κB luciferase reporter system was constructed and transiently transfected into HUVEC. Following transfection, HUVEC were pretreated with various concentrations of Vaspin (0~320 μg/L) before 10 μg/L TNF-α stimulation. The transcription activity of NF-κB was determined using luciferase reporter assay. The level of Akt phosphorylation was checked by Western blot. Expression levels of NF-κB downstream inflammatory cytokines IL-1 and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). mRNA and protein expression levels of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemotactic protein-1 (MCP-1) were determined by quantitative real-time PCR (qRT-PCR) and Western blot respectively. Results Vaspin inhibited TNF-α mediated activation of NF-κB and its downstream molecules (P<0.05). Vaspin significantly increased Akt phosphorylation in TNF-α stimulated endothelial cells (P<0.05). Conculsions Vaspin protected endothelial cells from TNF-α induced inflammation and insulin resistance by combination the inhibition of NF-κB, its downstream molecules and the upregulation of the PI3-kinase/Akt signal pathway.
    Effect of S1P on the glucose metabolism of LO2 liver cells insulin resistance model
    2015, 35(8):  1025-1030. 
    Asbtract ( 800 )   PDF (1957KB) ( 471 )  
    Related Articles | Metrics
    Objective To observe the impact of sphingosine kinase (SPK), catalysatee of sphingosine 1-phosphate (S1P), on the glucose metabolism of the LO2 liver cell insulin resistance model. Methods LO2 cells were induced with insulin to establish insulin resistance, and the MTT staining method to detect impacts of insulin on LO2 cells proliferation; the glucose-hexokinase method to detect remnant glucose concentration variations in the media stimulated with insulin of varying concentrations, and S1P’s impact on blood glucose absorption of cells in the insulin resistance model; the oil red O staining method to detect the extent of steatosis, and the fluorescence double staining method to identify the changes of mitochondrial ROS in LO2 cells; and Western blot method to detect SPK1 protein expression. Results Compared with the control group, insulin concentrations of 10, 100, and 1000 nmol/L insulin had no significant impact on glucose uptake capacity (P>0.05). Following a 48-h induction with 1000 nmol/L insulin, with decreased insulin sensitivity index and establishment of the insulin resistance model. Compared with the control group, liquid droplets area in the model group was found with an increase, and mitochondrial ROS was found with a significant increase. At the same time, the expression of SPK1 protein also showed a trend of increase. S1P, when added in the model group, could significantly promote cellular uptake of glucose. Conclusion The LO2 liver cell model of insulin resistance was established with insulin induction. S1P may be able to promote glucose metabolism, prompting S1P may serve as a new target spot for screening hypoglycemic drugs for type-II diabetes patients.
    SPD1672 protein influences teichoic acid synthesis and bacterial growth of Streptococcus pneumoniae
    2015, 35(8):  1031-1036. 
    Asbtract ( 446 )   PDF (1541KB) ( 390 )  
    Related Articles | Metrics
    Objective To identify the role of spd1672 gene in Streptococcus pneumoniae cell wall polysaccharide synthesis and proliferation. Methods spd1672-deletion strains were generated by the method of alternative inactivation in Streptococcus pneumoniae D39 and R6 strains. The thickness of capsular polysaccharide was detected by electron microscope,and teichoic acid was detected by Western blot. Furthermore,the growth of wild strains and spd1672-deletion strains in vitro were observed by absorption spectrophotometry. Results No difference was found in the thickness of capsule between wild strains and spd1672-deletion strains. However, the teichoic acid synthesis was significantly reduced in spd1672-deletion strains than that in wild strains. In addition, compared with wild strains, spd1672-deletion strains grow more slowly. Conclusion SPD1672 is a new virulence factor of Streptococcus pneumoniae, which may participate in the regulation of teichoic acid synthesis of Streptococcus pneumoniae and affect its growth in vivo.
    α-Lipoic acid in oxidative stress in hyperuricemia rats
    2015, 35(8):  1037-1041. 
    Asbtract ( 761 )   PDF (975KB) ( 582 )  
    Related Articles | Metrics
    Objective: To observe the effects of α-lipoic acid on oxidative stress and structure of vascular endothelial cell in hyperuricemia rats. Methods: 60 male Sprague-Dawley rats were divided into five groups, which were the control group, the model group and α-lipoic acid intervention groups .The model group and intervention groups were established to be hyperuricemia rats according to the reference. After three weeks, intervention groups were given different dose α-lipoic acid for fourteen days. At the end of experiment, serum UA, SOD ,GSH-Px, CAT and MDA were assayed. SOD and CAT protein expression of thoracic aorta were detected with Westernblot and thoracic aorta’s structure was observed with light microscope and electron microscope. Results:The activities of UA,SOD,GSH-Px and CAT of hyperuricemia rats were lower than the control group, the MDA level of hyperuricemia rats was higher than the control group, and the protein expression of SOD and CAT were lower than the control group(P<0.05). After α-lipoic acid intervention, UA and MDA of hyperuricemia rat were decreased among three intervention groups, SOD’s activities were increased in high group and medium group (P<0.05).The protein expression of SOD and CAT were increased in medium and high groups(P<0.05).It showed electron under electron microscope that hyperuricemia rat’s endothelial was edema, shedding and mitochondria swelling.After α-lipoic acid intervention,the medium and high dose groups were found that mitochondria had a transient increasing and edema endothelial cells was improved.Conclusion: α-lipoic acid could increase the activity and the protein expression of anti-oxidant enzymes, and relieve hyperuracemia rat’s oxidative stress,which could protect endothelial cells.
    Dyslipidemia in Buyi and Han population in Longli County Guizhou province
    2015, 35(8):  1042-1048. 
    Asbtract ( 510 )   PDF (691KB) ( 513 )  
    Related Articles | Metrics
    Objective To know characteristics of dyslipidemia in Buyi and Han residents in Longli County and to provide evidence for prevention strategies. Methods Stratified sampling was adopted to select 2 communities within the county seat of Longshan and 4 villages from 4 towns. 2929 healthy Buyi and Han residents aged between 20 to 80 years participated in this study. Their serum total cholesterol (TC), triglyceride (TG), high-density lipid-cholesterol (HDL-C), and low-density lipid cholesterol (LDL-C) were tested. Results The prevalence of dyslipidemia was 25.9% (31.1% for men, 22.0% for women, respectively). It was higher in men than in women (P<0.001). Compared with Buyi people, the prevalence was significantly higher in Han people (34.0%) then in Buyi was only 21.73% (P<0.001). The prevalence of high TG level was significantly higher in Han population (P<0.001), 13.2% in Buyi population and 22.6% in Han population, with 16.4% in the pooled sample. The prevalence of high TC level was significantly higher in Han population (P<0.05), 9.8% in Buyi population and 12.5% in Han population, with 10.7% in the pooled sample. The prevalence of low HDL-C level was significantly higher in Han population (P<0.001), 4.2% in Buyi population and 9.1% in Han population, with 5.8% in the pooled sample. The prevalence of high LDL-C level was significantly higher in Han population (P<0.05), 4.1% in Buyi population and 6.0% in Han population, with 4.8% in the pooled sample. Additionally, obesity and hypertension were the main risk factors for dyslipidemia among adults aged between 45 and 59 years. Conclusions High TG and hypercholesterolemia were the main components of dyslipidemia in Buyi and Han adults in Longli County. The prevalences of high TG, high TC, and high LDL-C were all higher than the results of 2010 national survey. Obviously, the prevalence of dyslipidemia was increasing over time. It suggested that attention should be paid for prevention and treatment of dyslipidemia in adults aged between 45 and 59 years.
    Clomiphene Citrate Inhibits rat endometrial proliferation and its mechanism
    2015, 35(8):  1049-1054. 
    Asbtract ( 742 )   PDF (1123KB) ( 551 )  
    Related Articles | Metrics
    Objective To explore the effect of Clomiphene Citrate on endometrial proliferation and the mechanism. Methods Animals were divided into CC group, five rats in each Drug were given for five days,while other groups included CC+E2、CC、CO groups,5 rats each and drugs were given for ten days. Cycle was observed , and intragastrical administration in proestrus was carried out for ten days with: clomiphene citrate (CC), Estradiol (E2), Normal Saline (Control,CO). Proteins of uterus were extracted for Western blot. Results In drug treated group uterine growth factor decreased significantly compared with the control group. After E2 co-administration with CC, its growth signal factor was increased than that of CC group, but not restored to normal level. Conclusion CC is attributed to the inhibitor of endometrial hyperplasia by inhibiting uterine growth factor. Combinding E2 and CC can alleviate such symptoms. The possible molecular mechanisms is associated with PI3K/AKT、JNK、NFKB and other related pathways.
    IL-2 promotes macrophage M1 polarization via the Jak3-Stat5 signaling pathway
    2015, 35(8):  1055-1060. 
    Asbtract ( 762 )   PDF (1077KB) ( 685 )  
    Related Articles | Metrics
    Objective To explore the effects and related mechanisms of Interleukin-2 (IL-2) on macrophage polarization. Methods Comparing with the recombinant mouse IL-4 (rmIL-4), rmIL-2 was used to treat the mouse macrophage cells RAW 264.7. Then, the cell markers of M1 and M2 expression were detected by Real-time PCR and Western blot. And the percentage of M1 or M2 macrophages was analyzed by flow cytometry. Additionally, the activation of Jak3 and Stat5 was also analyzed by Western blot. Results The expression of M1 maekers (IL-1β, IL-12, TNF-α and iNOS) was significantly up-regulated in RAW 264.7 cells after treated with IL-2. And the IL-2 treatment increased the percentage of M1 macrophages from 3.2% to 24.6%. Further, IL-2 significantly enhanced the phosphorylation of Jak3 and Stat5. Conclusions IL-2 could promote M1 polarization of macrophages, probably via the Jak3-Stat5 signaling pathway.
    Etanercept alleviates lumbar disc herniation-induced hyperalgesia and mRNA expressions of chemokine CCL2/CCR2 in DRG and spinal cord of rats
    2015, 35(8):  1061-1066. 
    Asbtract ( 536 )   PDF (1699KB) ( 473 )  
    Related Articles | Metrics
    Objective: To observe the effects of tumor necrosis factor-? (TNF-?) inhibitor etanercept on hyperalgesia of rats with lumbar disc herniation, as well as on the expression of chemokine CCL2 and its receptor CCR2 in DRG (dorsal root gangalion) and spinal cord. Methods: SD rats were randomly divided into six groups: Normal group (Control), Sham group (Sham), Nucleus pulposus transplantation Group (NP), NP + Vehicle group (Vehicle), NP + Etanercept 10 ?g (Etanercept 10 ?g), NP + Etanercept 100?g(Etanercept100?g).The mechanical withdrawal threshold (MWT) of the left hind paw of rats in different group was measured at 1 d before and different time points after the surgery. The real-time quantitative PCR was used to measure the mRNA expression level of TNF-α, CCL2/CCR2; Immunohistochemical staining was applied to investigate the expression of ED-1 and ATF3 in DRG. Result (1) Compared with Sham group, MWT in NP group was reduced significantly from1 d after the operation (P < 0.001), and lasted for more than 21 d (P < 0.001); (2) Intrathecal injection of etanercept (100 mg) attenuated the NP-induced mechanical allodynia at 2,3,4 d (P < 0.001); (3) Pretreatment of etanercept (100 mg ) inhibited the up-regulation of CCL2 and CCR2 mRNA in both DRG and spinal cord. Conclusion: Intrathecal injection of etanercept inhibits the neuropathic pain caused by the auto transplantation of nucleus pulposus. The mechanisms may be partly due to the inhibition of CCL2/CCR2 upregulation.
    Clinical significance and correlation of Yes-associated protein and β-catenin expression in gastric cancer
    2015, 35(8):  1067-1071. 
    Asbtract ( 510 )   PDF (981KB) ( 579 )  
    Related Articles | Metrics
    Objective To investigate the expressions and correlation of YAP andβ-catenin in the gastric carcinoma(GC) tissues and the paired normal gastric tissues. Methods Fluorescence quantitative PCR(RT-qPCR), immunocytochemistry staining and Western blotting were used to detect the mRNA and protein expressions of YAP and β-catenin in GC tissues and the paired normal gastric tissues,The correlations between the expressions and the clinicopathological characteristics of GC were analyzed statistically. Results The positive expression of YAP and β-catenin were respectively 72% (36/50) and 64% (32/50), and the positive expression of paired normal gastric tissues were 14% (7/50) and 20% (10/50), P<0.05; The mRNA and protein levels of YAP and β-catenin in GC tissues were higher than those in the paired normal tissues(P<0.05).Furthermore, the expression was obviously correlated to cell differentiation, lymph node metastases and clinical stage of GC( P< 0.05). The significantly positive correlation was found between the expressions of YAP and β-catenin in GC tissues(r=0.72, P<0.05). Conclusion The high expression of YAP and β-catenin coexist in GC tissues. It may be related to malignant transformation and abnormal proliferation of cells, which facilitates the occurrence and development of GC.
    Effects of exosomes derived from breast cancer cell on tumor angiogenesis and its mechanism
    2015, 35(8):  1072-1077. 
    Asbtract ( 497 )   PDF (1278KB) ( 419 )  
    Related Articles | Metrics
    Objective To study the effects of breast cancer cell exosomes on HUVECs,and to explore the possible mechanism. Methods Exosomes were prepared from the supernatants of MDA-MB-231 cells by density gradient ultracentrifugation. HUVECs proliferation after treated with Exosomes was measured by MTT. FACS was used to detect the distribution of HUVECs cell cycle. Transwell was used to HUVECs migration. Matrigel glue was used to detectd changes in tube formation.PCR was used to detect the expression of EGFR and VEGF mRNA.ELISA and Western blot was used to detect EGFR and the expression of its downstream protein,such as ERK & Akt, and VEGF / VEGFR2.Results Exosomes promoted HUVECs proliferation in a time-and dose-dependent manner(P<0.05),and HUVECs in S-phase G1-phase and the rate of G1/S phase of the cell cycle (P<0.05). The migration and capability of tube formation of HUVECs were enhanced by Exosomes(P<0.05).And Exosomes promoted the expression of EGFR, phospho-ERK & Akt protein, the secretion of VEGF protein increased, and the VEGF / VEGFR2 protein in HUVECs increased.Conclusion Breast cancer cell Exosomes promote HUVECs proliferation,migration and the capability of tube formation, possibly via the expression of EGFR and activating the MAPK/ERK,PI3K/Akt and VEGF/VEGFR2.
    To analysis differencied gene expression between mesenchymal stem cells and hepatocyte-like transformed cells
    2015, 35(8):  1078-1082. 
    Asbtract ( 544 )   PDF (991KB) ( 355 )  
    Related Articles | Metrics
    Objective To analysis of differential on gene expression profiles between rat bone marrow mesenchymal stem cells and hepatocyte like cells which were directional differentiated by gene expression microarray technology. Method To make the rat’s MSCs directional differentiation into hepatocyte-like cells this procedure was repeated 3 times, to amplified respectively MSCs and hepatocyte-like cell total RNA, fluorescent labeled Cy3 probe. And then basing on fluorescence in situ hybridization, scanning, screening the differential information with GO and pathway analysis. The results were validated by RT-PCR. Results The test results appeared to MSCs Vs HLCs 839 genes was different , among 448 genes up-regulated, 391 genes down –regulated,363 genes with biological process annotation, 377 genes with cellular components annotation, 364 genes with molecular function annotation. The Pathway analysis results revealed 45 pathways had significant changed among the 273 Pathways, 275 differentially expressed genes involved in those pathway, including 122 up-regulated genes and 153 down regulated genes. Constructing gene regulatory network through those differential gene expression, according to the degree in the network and selected 5 key gene: Pkm2, Nt5e, Fos, Adcy3, Itga7. Conclusion In this procedure that MSCs was induced and differentiate into HLCs in vitro, These regulate gene expression in transformed cells just as the same as liver cells, such as: proliferation, differentiation, apoptosis, metabolism and regulation are closely related.
    Preparation of LINE1-ORF1 Antibody and detection of LINE-1 retrotransposition during neural progentitor cells differentiation
    Jingjing Lu
    2015, 35(8):  1083-1088. 
    Asbtract ( 594 )   PDF (1208KB) ( 468 )  
    Related Articles | Metrics
    Objective To explore endogenous LINE-1 expression during Neural progenitor cells (NPCs) differentiation. Method recombinant LINE-1 ORF1 protein was expressed in bacteria, followed by purification, and the purified protein was used to immunize rabbits to produce anti-ORF1 polyclonal antibody. The antibody was used to detect LINE-1 retrotransposition during neural progenitor cells (NPCs) differentiation by Western blotting. Result The anti-ORF1 antibody possessed high sensitivity and specificity, and observed the variability of LINE-1 retrotransposition in different eukaryotic cell lines. Using anti-ORF1 antibody to detect LINE-1 ORF1 protein level during NPC differentiation, it was found that when stem cells commits to NPCs, LINE-1 retrotransiposition increases in the early stage and decline in the late stage. Conclusion LINE-1 retrotranspose increases upon neuronal commitment, suggested LINE-1 play a pivotal role in neural development.
    IL-1β induced endoplasmic reticulum stress increases human chondrocyte apoptosis and the mechanism
    2015, 35(8):  1089-1093. 
    Asbtract ( 695 )   PDF (924KB) ( 472 )  
    Related Articles | Metrics
    Objective To analysis the effects of inflammation factors (IL-1β, TNF-α) on endoplasmic reticulum stress (ERS) and the association with osteoarticular chondrocyte apoptosis. Methods Osteoarticular cartilage tissues were collected from normal and patients with OA (20 cases for each group). RT-PCR were performed to measure the mRNA level of IL-1β, TNF-α, GRP78 and CHOP in cartilaginous tissues. Western blot was used to evaluate the expression of GRP78, CHOP, ATF4 and caspase-3 in chondrocytes. The apoptosis of chondrocyte was analyzed by TUNEL. Results Compared with control, mRNA levels of IL-1β, TNF-α, GRP78 and CHOP in OA were significantly higher (P<0.01), while the high expression of IL-1β was positively correlated to GRP78 and CHOP (P<0.05). In vitro, GRP78, CHOP, ATF4 expression and chondrocyte apoptosis significantly increased in response to the treatment of IL-1β (2 ng/L) (P<0.01). In addition, the expression of GRP78, caspase-3 and chondrocyte apoptosis were significantly higher after incubation with TNF-α (P<0.01). Conclusion 2 ng/L and higher dosage of IL-1β triggered ATF4-CHOP-mediated ERS to induce chondrocyte apoptosis.
    CD44 promotes the proliferation and adhesion of human vascular endothelial cells
    2015, 35(8):  1094-1099. 
    Asbtract ( 536 )   PDF (975KB) ( 347 )  
    Related Articles | Metrics
    Objective To study the effect and mechanism of CD44 in endothelial cell proliferation and adhesion. Methods The pcDNA3.1 vectors were constructed to upregulate the CD44 gene of Human umbilical vein endothelial cells (HUVEC); Akt siRNA and PECAM1 siRNA were used to knockdown the gene of Akt and PECAM1, respectively. Cell proliferation was measured by MTT assay, cell adhesion rate was measured by cell counting, PECAM1 mRNA levels were detected by RT-PCR, and Western blot was used to determine the protein levels of Ki67, PECAM1 and Akt phosphorylation. Results CD44 promoted HUVEC proliferation, increased Ki67 expression and promoted Akt phosphorylation (all P<0.05); while, Akt siRNA decreased the CD44-induced cell proliferation (P<0.05). Moreover, CD44 promote HUVEC adhesion (P<0.05), and increased the mRNA and protein levels of PECAM1 (all P<0.05); moreover, PECAM1 siRNA impaired CD44-induced cell adhesion. Conclusion CD44 promotes the proliferation of HUVEC cells by activating the Akt signaling pathway; CD44 promotes cell adhesion by increasing the mRNA and protein levels of PECAM1.
    Expression and clinical significance of FOXM1 in breast cancer tissues and MCF-7 cells
    2015, 35(8):  1100-1105. 
    Asbtract ( 684 )   PDF (1288KB) ( 482 )  
    Related Articles | Metrics
    Objective To study the expression of FOXM1 in human breast cancer, analyze the relationship between FOXM1 and clinical pathological features and explore the role of FOXM1 in cell proliferation. Methods FOXM1 expression in breast cancer tissues was detected by immunohistochemistry (IHC) on 147 parffin-embedded slices. χ2 test was used to analyze the relationship of FOXM1, clinical parameters, as well as Ki-67. What's more, Western Blot was used to analyze the role of FOXM1 in cell cycle process during serum starvation and refeeding. At last, the expression level of FOXM1 was knocked down to analyze the alteration of MCF-7 cell vitality. Results FOXM1 was highly expressed in breast cancer. The expression of FOXM1 was consistent with the level of Ki-67. FOXM1 expression in breast cancer was significantly correlated with Her-2, lymph node status, as well as Ki-67 (P<0.05). With serum starvation for 72 hours and refeeding with the DMEM medium contain 5% fetal bovine serum in MCF-7 cells, the proliferation ability was enhanced (P<0.05). While interferenced with FOXM1, the proliferation ability was inhibited (P<0.05). Conclusions The abnormal expression of FOXM1 might be closely related to the initiation and progression of breast cancer. FOXM1 might be an indicator to predict the prognosis and serve as a potential target for therapy in breast cancer.
    A clinical report of 13 patients with filum terminale ependymal neoplasm
    2015, 35(8):  1106-1109. 
    Asbtract ( 641 )   PDF (851KB) ( 554 )  
    Related Articles | Metrics
    Objective To evaluate the clinical features, strategy of surgery, and prognosis of the patients with filum terminale ependymal neoplasm. Methods The clinical features, imaging findings, pathologic manifestation, operative details and prognosis of 13 patients with filum terminale ependymal neoplasm operated in the department of neurosurgery between 2009 and 2014 were retrospectively reviewed. Results The most common location of the tumor was in T12-L3, with the length between 1.5cm and 11 cm (average 4.1cm). Seven of 13 patients (54%) were reported as WHO grade I myxopapillary ependymoma, the other 6 patients (46%) were reported as WHO grade II ependymoma. Surgically gross total resection (GTR) was obtained in 10 patients without any recurrence in the follow up period. The subtotal resection (STR) was obtained in the other 3 patients, in which 2 patients with WHO grade II ependymoma relapsed in the follow up period although adjuvant radiotherapy was adopted post-operatively. Except these 2 relapsed patients, the modified Mccormick Scale of the other 11 patients improved at least 1 level or remained at the pre-operative levels. Conclusions Gross total resection (GTR) is the most efficient method for the ependymal neoplasms of filum terminale.
    A case report of surgical treatment of idiopathic intracranial hypertention
    2015, 35(8):  1110-1112. 
    Asbtract ( 430 )   PDF (590KB) ( 383 )  
    Related Articles | Metrics
    Idiopathic intracranial hypertension is a disease which has a low incidence and has no clear indication for its diagnosis and treatment. In addition, there is also little report on its surgical treatment. Here we report a case of which the curative effect turned out to be undesired after conservative physical treatment and then the symptom aggravated gradually, finally , we took operation based on bilateral decompressive craniectomy of which the result was favorable and the patient’s sight was restored. Then we took a nine-year long follow-up survey which proved the treatment being effective and the disease is under control.
    Maresin-1 attenuates acute lung ischemia-reperfusion injury in mice
    2015, 35(8):  1116-1118. 
    Asbtract ( 441 )   PDF (881KB) ( 471 )  
    Related Articles | Metrics
    The Progress of inducement and mechanism during the development of pancreatic cancer
    2015, 35(8):  1122-1125. 
    Asbtract ( 101 )   PDF (542KB) ( 463 )  
    Related Articles | Metrics
    Environmental factors and lifestyle have become a hot public concern in the inducement of pancreatic cancer, disease and individual factors can also provide some guidance for high-risk groups. The mechanism during the pancreatic cancer have complex signaling networks, including such as MAPK, Wnt, Notch, Hedgehog and PI3K / AKT signaling pathway.
    The non-antibiotic effects of azithromycin and its clinical application progress
    Jin TONG
    2015, 35(8):  1126-1129. 
    Asbtract ( 154 )   PDF (529KB) ( 588 )  
    Related Articles | Metrics
    Azithromycin is a typical macrolide antibiotic with a 15-membered lactone ring and its non-antibiotic roles have been attracted increasingly great attention in recent years. The purpose of our present review is to summary the various non-antibiotic effects of azithromycin, including activities of anti-inflammation, immunomodulation, biofilm damage, regulation of airway mucus, change of macrophage phenotype and regulation of liquid electrolyte among airway surface, and simultaneously, its beneficial effects of long-term clinical application in treatment of lung disease with chronic infection with low dose as well as its nebulization efficiency.
    The meaning of proteomics in the biological characteristics of colorectal neoplasms
    Xiao-Ling CHAI
    2015, 35(8):  1130-1133. 
    Asbtract ( 91 )   PDF (526KB) ( 613 )  
    Related Articles | Metrics
    Discussing the mechanism of colorectal cancer development, the mechanism of invasion and metastasis, the change characteristics of tumor cells proliferation and apoptosis, anti-tumor drug resistant mechanism by proteomics technology, which supply a new thought for colorectal neoplasms prevention, early diagnosis and individualized treatment.
    Advances of multiplex ligation-dependent probe amplification technology on detection of gene deletions/duplications
    2015, 35(8):  1134-1138. 
    Asbtract ( 162 )   PDF (1056KB) ( 438 )  
    Related Articles | Metrics
    The multiplex ligation-dependent probe amplification (MLPA) technology used in detection of gene deletions/duplications not only helps in understanding the molecular mechanisms underlying the development of cancer, but also provides important information for disease diagnosis and prognosis. Currently, MLPA becomes a hotspot to be applied in testing tumor related gene deletions/duplications mutations.
    The joint cultivation of pathological diagnosis and research skills for medical postgraduates of pathology
    2015, 35(8):  1139-1141. 
    Asbtract ( 88 )   PDF (427KB) ( 438 )  
    Related Articles | Metrics
    Pathology is the bridge between the basic and clinical medicine, and the training of medical postgraduates of pathology should be different from the other medical science, and we should pay attention to the training of pathological diagnosis and research skills equally. Here, based on the cultivation in our department, we generated the joint cultivation of pathological diagnosis and research skills for postgraduates of pathology. An effective approach for training the medical postgraduates of pathology is helpful to increase the quantity and quality of clinical pathologist, and improves the development of pathology in our country.
    On the fundamentality to foster scientific theory formation ability of medical postgraduates
    2015, 35(8):  1142-1144. 
    Asbtract ( 85 )   PDF (444KB) ( 349 )  
    Related Articles | Metrics
    How to improve the scientific research capability is still a key question for the education of medical postgraduates. Presently, medical collages generally pay more attention to the education of experimental skills than scientific theory formation capability of medical postgraduates. Due to the fact that no scientific theory novelty will inevitably result in none of scientific experiment novelty, it should be aware that training of scientific theory formation capability is essential for medical postgraduates. An effective approach for improving scientific theory formation capability of medical postgraduates may be training of their new scientific hypothesis formation capability.
    Preliminary exploration into rare disease teaching in medical genetics
    2015, 35(8):  1145-1147. 
    Asbtract ( 115 )   PDF (503KB) ( 355 )  
    Related Articles | Metrics
    In clinic, rare disease practice faces several problems, such as, frequent diagnosis errors, non-standardized treatment, and ineffective in preventing recurrence. In this paper, from the perspective of strengthening the rare disease teaching, we preliminarily explored how to improve the medical students’ cognitive level of rare disease by taking multiple measures, such as, delivery of selected teaching contents, application of diversity teaching methods and participation in clinical practice.
    Training the innovative ability of medical undergraduates with teaching reform and scientific research as the carrier
    2015, 35(8):  1148-1150. 
    Asbtract ( 103 )   PDF (473KB) ( 470 )  
    Related Articles | Metrics
    Cultivating medical undergraduate students’innovation ability is the core of quality education. The cultivation of innovative ability covers the independent thinking, cultivating creative thinking, cultivating creative thinking, team work spirit,and the cultivation of research quality,etc.In the process of teaching content and methods reform,our group found the combination of teaching and research can cultivate the students' innovation consciousness and innovation ability.
    Impact of clinicians’ stress status on the professionalism development of 8-curriculum medical students
    2015, 35(8):  1151-1154. 
    Asbtract ( 115 )   PDF (510KB) ( 345 )  
    Related Articles | Metrics
    Objective To study the stress status of clinical physicians, help medical students in the 8-year program form correct perspectives of their occupation, and eventually facilitate institution of professionalism education. Methods Interview-based medical student questionnaires on professionalism were dependently designed. Random sampling was used. Results The clinical physicians reported to feel under considerable and persistent stress. No statistically significant difference in degree of stress recognition is observed in association with their current career status or reasons for occupational choices. However, there is statistically significant difference in degree of stress recognition related to their wills of being physicians (P<0.05), showing that more determined physicians tend to feel less pressure. Conclusions Reinforcement in stress recognition and surveillance is recommended in 8-year medical education. Further work should be done to increase the student’s interest in their occupation, enhance their occupational determination, and improve communication between schools and students’ families.