Circulating vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor (VEGF) levels in patients with colorectal carcinoma were determined in order to assess their clinical significance as a diagnostic tool for monitoring lymph node metastasis. In 66 patients with colorectal carcinoma and 30 healthy controls, circulating VEGF-C and VEGF levels were assessed by using enzyme-linked immunosorbent assay (ELISA). Serum VEGF-C and VEGF levels were higher in patients with colorectal carcinoma than in healthy controls. Patients with lymph node metastasis had higher serum VEGF-C and VEGF levels than those without lymph node metastasis. The levels of VEGF-C and VEGF were higher in the invasion group than in the non-invasion group. Serum VEGF-C levels reached a sensitivity of 81% and a specificity of 76% with a cutoff value of 1438.0 pg/mL, whereas VEGF levels reached 72% sensitivity and 74% specificity at 240.2 pg/ mL. If 66 patients were divided into 4 groups according to the combined determination of VEGF-C and VEGF levels, the positive predictive value was 85.3%, the negative predictive value was 94.6%, and accuracy was 93.7%. It was suggested that circulating VEGF-C levels might provide additional information for distinguishing the absence from presence of lymph node metastasis in patients with colorectal carcinoma. The combined determination of VEGF-C and VEGF levels could be used as an important index for preoperatively clinical stage of colorectal carcinoma.

Objective To measure circulating vascular endothelial growth factor-C(VEGF-C) levels in(patients) with colorectal carcinoma,and assess the clinical significance in diagnosis of lymph node metastasis.Methods Sixty-six patients with colorectal carcinoma and 30 healthy control patients were included in this study.Circulating VEGF-C and VEGF levels were assessed by enzyme-linked immunosorbent assay.Results Serum VEGF-C and VEGF concentration was higher in patients with colorectal carcinoma than in healthy control patients(P

[Objective]To discuss the pathological typing of posterior longitudinal ligament(PLL) in cervical spondylotic myelopathy.[Method]Data of pathological typing and resection methods of PLL were reviewed in 87 patients with cervical spondylotic myelopathy.[Result]The degeneration of the posterior longitudinal ligament(DPLL) was divided into single-DPLL(n=34,39.1%) and proliferation-DPLL(n=53,60.9%) by the results of resecton and pathological studies.The proliferation-DPLL was subdivided into hyperplasy-DPLL(n=26,29.9%),accretion-DPLL(n=12,13.8%)and ossification-DPLL(n=15,17.2%).[Conclusion]The posterior longitudinal ligament can thoroughly be resected in cervical spondylotic myelopathy combined with single-DPLL or with hyperplasy-DPLL.In cervical spondylotic myelopathy combined with accretion-DPLL or ossification-DPLL,complete decompression can be obtained by isolating the accretion and the ossification-chondrification of DPLL.

Aim To explore the effect of N-acetyl-L-cysteine ( NAC ) on β amyloid peptide 25 - 35 ( Aβ25-35 )-induced the increase of calpain activity and its possible mechanism. Methods The activity of cal-pain was induced by 20μmol·L-1 Aβ 25-35 in primary cortical neuron. Neurons were incubated in the absent or present Aβ25-35 , or pre-incubated NAC ( 10 mmol ·L-1 ) , then co-incubated with Aβ25-35 . The meas-urement of calpain activity, H2 O2 level and mitochon-drial membrane potential was performed on a micro-plate fluorometer. The ATP level was detected using a luciferin/luciferase based ATP assay kit. Results In Aβ25-35 treated group, the activity of calpain and H2 O2 was obviously higher than that in control group. How-ever, in neurons pre-incubated in NAC and then co-in-cubated in Aβ25-35 , the calpain activity and H2 O2 level were significantly decreased compared with that in Aβ25-35 group. Upon Aβ25-35 exposure for 12 h, corti-cal neurons showed a significant decrease in mitochon-drial membrane potential and ATP level when com-pared to the control group. Pre-treatment with NAC showed an increase in mitochondrial membrane poten-tial and ATP level as compared to neurons treated with Aβ25-35 alone for 12h. Conclusion This result sug-gests that NAC can attenuate calpain activity induced by Aβ25-35 through protecting mitochondria.

BACKGROUND:Posterior cervical open-door expansive laminoplasty is one of the simple and effective methods to treat cervical spinal diseases, has satisfactory results but low complications. However, the imbalance of sagittal plan, loss of lordosis or axial pain is often reported recently. OBJECTVE:To analyze the correlation between cervical sagittal alignment and clinical outcomes after laminoplasty. METHODS:Between January 2011 and June 2015, 122 cases of cervical spinal disease, who were treated with open-door expansive laminoplasty with mini-titanium plate, were retrospectively analyzed. Clinical outcomes were evaluated by Japanese Orthopaedic Association, Neck Disability Index and Visual Analogue Scale. Radiographic results were assessed by C2-7 Cobb angle, C2-7 sagittal vertical axis and C7 slope. The correlation between sagittal alignment and clinical outcomes were analyzed. RESULTS AND CONCLUSION:(1) Al patients were fol owed up for 7-32 months. (2) Japanese Orthopaedic Association, Neck Disability Index and Visual Analogue Scale scores were improved in the final fol ow-up (al P<0.001). No significant difference in upper limb Visual Analogue Scale scores was determined (P=0.142). In the final fol ow-up, C2-7 sagittal vertical axis increased (P=0.036), but neither the C2-7 Cobb angle nor the C7 slope significantly changed (P=0.092, P=0.184). (3) There were no correlations between sagittal alignment parameters (C2-7 Cobb angle, C2-7 sagittal vertical axis and C7 slope) and clinical outcomes (Japanese Orthopaedic Association, Neck Disability Index and Visual Analogue Scale) (al P>0.05). (4) These findings indicated that posterior cervical open-door expansive laminoplasty with mini-titanium plate can significantly improve the neurological function of patients. However, there is no correlation between cervical sagittal alignment and clinical outcomes.

Aim To explore the possible protective effect of ginsenoside Rg1 on oligomeric Aβ1-42 induced apoptosis and its possible mechanism. Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neurons. Cells were incubated in the absence or presence of Aβ, or co-incubated in sp600125 with Aβ, or pre-incubated in ginsenoside Rg1 then co-incu-bated in Aβ. The p-JNK, JNK, caspase-3 activity and TUNEL-positive cells were detected. Results In Aβ1-42 treated group, the ratio of p-JNK/JNK level was increased more than that in non-treated group for 15 min. However, in neurons preincubated with (2. 5, 5, 10 μmol·L-1 ) ginsenoside Rg1 and then co-incuba-ted with 5 μmol·L-1 oligomeric Aβ1-42 , the p-JNK/JNK ratio, caspase-3 activity and TUNEL positive neu-rons were significantly decreased compared with those of Aβ1-42 treated group. Conclusion Ginsenoside Rg1 can attenuate the oligomeric Aβ1-42-induced apop-tosis by JNK pathway.

ObjectiveTo explore the risk factors for the prognosis of respiratory failure in neonates with gestational age≥34 weeks. MethodsA total of 143 hospitalized neonates with respiratory failure who had gestational age≥34 weeks were enrolled from Jan. 2011 to Jun. 2013. According to the outcome, the neonates were divided into good prognosis group and poor prognosis group. The risk factors for the prognosis of respiratory failure were screened by univariate analysis and mul-tivariate binary logistic regression model.ResultsAmong the 143 neonates, 105 neonates had good prognosis and 38 neonates had poor prognosis. Univariate analysis showed that the mode of delivery, small for gestational age, 5 minutes Apgar score <7, and with primary disease being pneumonia/sepsis were associated with a poor prognosis. The differences were statistically signif-icant (P<0.05). Furthermore, the multivariate binary logistic regression model showed that, small for gestation age (OR=23.87, 95%CI:3.149-180.9) and pneumonia/sepsis (OR=2.996, 95%CI:1.514-5.928) were the independent factors of poor prognosis. ConclusionsSmall for gestation age and primary diseases being pneumonia/sepsis are the independent factors inlfuencing prog-nosis of respiratory failure in neonates born at a gestational age≥34 weeks.

Objective To systematically assess the efficacy of memantine on moderate to severe Alzheimer's disease (AD).Methods With the evaluation method of the Cochrane system,searches were made in the Cochrane Library,MEDLINE,Embase,Forest Laboratories,CNKI,Wanfang Data,and VIP Data up to February 2013 for double blind,randomized,and placebo-controlled trials (RCTs) evaluating the efficacy of memantine for moderate to severe AD.A meta-analysis of included clinical trials was conducted using the Revman 5.2 software to evaluate the efficacy of memantine on overall clinical status,cognitive function activities of daily living,and behavioral and psychological disturbances.Results A total of 8 RCTs were included (2 527 patients with moderate to severe AD).Results of the meta-analysis showed that,for patients with moderate to severe AD,memantine had better efficacy than placebo on overall clinical status,cognitive function,and activities of daily living (MD=-0.24,95％CI:0.340.15;SMD=-0.26,95％CI:-0.340.18;SMD=-0.13,95％CI:-0.21-0.05),but there was no significant difference in efficacy on behavioral and psychological function between memantine and placebo (P =0.08).Analysis of subgroups showed that memantine had better efficacy than placebo on cognitive function in moderate AD patients (SMD =-0.22,95％CI:-0.37 0.06) and on overall clinical status,cognitive function,and activities of daily living in severe AD patients (MD-0.29,95％CI:-0.40 0.18;SMD=-0.31,95％CI:0.46-0.15;SMD=-0.16,95％ CI:-0.25 0.06;MD=-3.13,95％ CI:-4.88-1.39;respectively).Conclusions Memantine has efficacy on overall clinical status,cognitive function and activities of daily living in patients with moderate to severe AD,especially in patients with severe AD.

Objective To investigate the possible effect of ginsenoside Rg1 and oligo Aβ1-42 on PKA/CREB pathway.Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neuron.Neurons were incubated with or without glutamate,or incubated in Aβ,or pre-incubated in Rg1 and then co-incubated in Aβ.The proteins of p-CREB,t-CREB,PKA Ⅱ α and BDNF were detected by Western blot.Results After the treatment with Oligo Aβ1-42 for 2 h,the p-CREB/t-CREB level induced by glutamate was obviously lower (P＜ 0.001).However,in neurons pre incubatedwith 2.5,5.0,10.0 μmol/L of ginsenoside Rg1 and then co-incubated with 5μmol/L of oligo Aβ1-42,the p-CREB/t-CREB induced by glutamate was significantly increased as compared with that of Aβ1-42 group (P＜0.05).Upon Aβ1-42 exposure for 2 h,cortical neurons showed a statistically significant increase in PKA Ⅱ α as compared to the control group (P ＜ 0.001).Pre-treatmentwith varying doses of ginsenoside Rg1 (2.5,5,10μmol/L) showed a decrease in PKA Ⅱ α as compared to neurons treated with Aβ1-42 alone for 2 h (P＜0.001).Furthermore,BDNF level significantly increased in Rgl-pretreated cells as compared to cells treated with Aβ1-42 alone for 24h (P＜0.05).Conclusions Ginsenoside Rg1 attenuates the oligo Aβ142 inhibition of PKA/CREB pathway.

Objective To probe into the gene therapy of psoriasis using antisense oligonucleotides to attenuate the expression of K14 gene and protein in keratinocytes and evaluate the inhibitory effects of liposome conjugated antisense oligonucleotides on the proliferation of keratinocytes. Methods The antisense, sense and mismatched oligonucleotides for K14 gene were synthesized and conjugated with lipofectin respectively. Finally they were subsequently transfected into cultured keratinocytes in vitro. The expression of K14 gene was tested by reverse transcription polymerase chain reaction (RT-PCR). The expression of K14 protein was measured by immunohistochemistry. The variation of cell growth cycle was detected by flow cytometry. Results The expression of K14 gene and protein was markedly decreased in keratinocytes treated with K14 antisense oligonucleotides. The cell growth cycle was inhibited effectively by antisense oligonucleotides with lipofection, but not by sense and mismatched oligonucleotides. Conclusions Antisense oligonucleotides conjugated with lipofectin might be a hopeful method to inhibit the proliferation of keratinocytes by inhibiting the expression of K14 mRNA and protein.