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Objective@#To observe the expressions of periostin (Postn) in colon cancer tissues and cells, and to investigate its biological effect and mechanism in colon cancer cells.@*Methods@#Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to detect the expressions of Postn, let-7a and miR-98 in 20 pairs of colon cancer tissues and adjacent normal tissues, colon cancer cell lines including SW480, HT-29, HCT-116 and human normal colon epithelial cell NCM460. Small interfering RNAs (siRNAs) of Postn, pcDNA3.1-Postn plasmids, let-7a mimic and its negative control let-7a mimic-NC, miR-98 mimic and its negative control miR-98 mimic-NC were transfected into HCT-116 cells. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H tetrazolium bromide (MTT) was used to detect cell viability. Flow cytometry was used to detect cell apoptosis. Luciferase reporter gene assay was used to determine the targeting relationship between miRNAs and Postn.@*Results@#Compared with adjacent normal tissues, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in colon cancer tissues. Compared with NCM460 cells, Postn expression was up-regulated (P<0.05) while let-7a/miR-98 expression was down-regulated (P<0.05) in SW480, HT-29 and HCT-116 cells. In colon cancer tissues, the expression of Postn was negatively correlated with the expressions of let-7a and miR-98 (r=-0.69, P<0.001; r=-0.80, P<0.001). Inhibition of Postn in vitro reduced the viability of HCT-116 cells [(53.73±7.63)%, P<0.05], increased the apoptotic rate [(22.88±3.40)%, P<0.05], enhanced the expression of epithelial-mesenchymal transition (EMT) marker E-cadherin (2.44±0.39, P<0.05), while down-regulated the expressions of N-cadherin and Vimentin (0.44±0.07 and 0.38±0.06, P<0.05). Overexpression of Postn in vitro enhanced the cell viability of HCT-116 cells [(134.41±8.82) %, P<0.05], decreased the expression of E-cadherin (0.55±0.09, P<0.05), increased the expressions of N-cadherin and Vimentin (2.93±0.42 and 2.24±0.34, P<0.05), but had no effect on the apoptotic rate (P>0.05). Overexpression of let-7a or miR-98 partially reversed the biological effects of Postn overexpression in colon cancer cells, which implicated that Postn was a target gene of let-7a/miR-98.@*Conclusions@#Postn is a cancer-promoting molecule of colon cancer, and inhibition of Postn expression can increase the apoptotic rate of colon cancer cells and repress EMT. Postn expression and function is regulated by let-7a/miR-98.
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Objective To investigate the clinical effect of 125I seeds implantation on bone metastasis from radioactive iodine-refractory differentiated thyroid carcinoma (RAIR-DTC).Methods A total of 9 RAIR-DTC patients with bone metastases (4 males,5 females,age range:42-87 years) between April 2014 and December 2016 were enrolled in this prospective study.Treatment plan was developed through treatment planning system (TPS).125I seeds implantation was performed under CT guidance.After 2 and 4 months,metastasis size,serum thyroglobulin (Tg) and verbal rating scale (VRS) pain score changes were recorded.Paired t test and two-sample t test were used for data analysis.Results VRS pain score decreased 2 months post-treatment comparing with that before treatment (2.56±0.88 vs 5.22±2.44;t =4.28,P<0.01).VRS pain score at 4 months post-treatment was 1.78±0.83,which was lower than that at 2 months post-treatment (t =3.48,P<0.01).The maximum tumor diameters before the implantation and 2 months post-treatment were (6.47± 1.84) cm and (5.08±2.11) cm,respectively (t =9.14,P<0.01).The maximum tumor diameter at 4 months post-treatment showed a decreasing trend but it was not statistically different compared to that at 2 months post-treatment:((4.52±2.16) cm;t =2.19,P>0.05).Serum Tg level reduced 2 months after the implantation (lgTg:2.71±0.85 vs 2.94±0.82;t =4.82,P<0.01).Serum Tg level at 4 months post-treatment (lgTg:2.56±0.81) was lower than that at 2 months post-treatment (t =2.69,P<0.05).Conclusions 125I seeds implantation is an effective method for treating bone metastasis from RAIR-DTC.It can help to shrink bone metastasis,alleviate pain and improve patients' quality of life.
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<p><b>OBJECTIVE</b>To study the expression of myeloid-derived suppressor cells (MDSC) in peripheral blood of patients with rectal carcinoma and to preliminarily explore its clinical significance.</p><p><b>METHODS</b>Blood samples from 76 rectal carcinoma patients who underwent surgery in Department of General Surgery, The Affiliated Cancer Hospital, Zhengzhou University between June and October 2013 were collected before operation, postoperative day 10 and 2 years after operation respectively. Flow cytometry was used to detect MDSC percentage in peripheral blood of 76 rectal carcinoma patients and 40 healthy people. The change of MDSC percentage in peripheral blood of rectal carcinoma patients after treatment was investigated. Furthermore, the relationship of peripheral blood MDSC percentage with clinicopathological characteristics was examined.</p><p><b>RESULTS</b>Preoperative MDSC percentage in peripheral blood of 76 rectal carcinoma patients [(3.52±0.68)%] was higher than that of 40 healthy people[(0.92±0.21)%], with significant difference (t=3.026, P=0.005). Preoperative MDSC percentage in peripheral blood of rectal carcinoma patients was significantly related with histological classification (t=2.453, P=0.018), depth of tumor invasion (t=2.051, P=0.035), lymph node metastasis (t=2.328, P=0.022), TNM stage (t=2.529, P=0.016). Univariate analysis showed that TNM stage, histological classification, lymph node metastasis, preoperative MDSC percentage in peripheral blood were the prognostic factors in rectal carcinoma. Multivariate analysis showed that TNM stage (HR=2.535, 95%CI: 0.851 to 4.160, P=0.038) and preoperative MDSC percentage in peripheral blood (HR=3.651, 95%CI: 0.877 to 14.263, P=0.031) were independent prognostic factors of rectal carcinoma. MDSC percentage in peripheral blood of rectal carcinoma patients decreased significantly on the postoperative 10-day [(2.41±0.46)%] compared to that before operation [(3.52±0.68)%], whose difference was statistically significant (t=1.778, P=0.043). During follow-up, tumor recurrence or metastasis was found in 23 patients. MDSC percentage in peripheral blood of rectal carcinoma patients with recurrence or metastasis [(4.37±1.23)%] was higher than that of rectal carcinoma patients without recurrence or metastasis [(2.36±0.35)%] two years after operation, with statistically significant difference (t=1.982, P=0.039).</p><p><b>CONCLUSIONS</b>MDSC percentage in peripheral blood of rectal carcinoma patients is significantly elevated compared to that of healthy people. Increased MDSC percentage indicates poor prognosis and tumor progression in rectal carcinoma patients. Measurement of peripheral blood MDSC percentage may have a potential clinical value in prognosis prediction of rectal carcinoma.</p>
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<p><b>OBJECTIVE</b>To predict and identify the target gene of miR-145, and to explore the underlying mechanism of the inhibition of miR-145 on drug resistance to Oxaliplatin (L-OHP) in human colorectal cancer cells.</p><p><b>METHODS</b>L-OHP-resistant human colorectal cancer cell line (HCT116/L-OHP) was established in vitro by exposing to increased concentrations of L-OHP in cell culture medium. MiR-145-mimics and its negative control (NC-miRNA) were transfected into HCT116/L-OHP cells using liposome to establish HCT116/L-OHPover-expressing miR-145 and HCT116/L-OHP. The target genes of miR-145 were predicted by bioinformatic analysis, and validated by dual luciferase activity assay. After determination of G protein coupled receptor 98(GPR98) as target gene, corresponding plasmids were constructed and transfected to establish HCT116/L-OHPover-expressing GPR98 and HCT116/L-OHP. HCT116/L-OHP cells over-expressing both GPR98 and miR-145 (HCT116/L-OHP) were acquired through modification of the binding sites of GPR98 cDNA with miR-145. CCK-8 assay was used to assess the proliferation (A value) and sensitivity to L-OHP (the lower the IC50, the stronger the sensitivity) in HCT116/L-OHP cells. Real-time quantitative PCR was used to measure the mRNA expression of miR-145 and GPR98. Western blot was used to examine the protein expression of GPR98 and drug-resistant associated protein, such as P-glycoprotein (gp), multiple drug-resistance protein 1(MRP1), cancer-inhibition gene PTEN.</p><p><b>RESULTS</b>HCT116/L-OHP cell line was successfully established with ICof (42.34±1.05) mg/L and miR-145 mRNA expression of 0.27±0.04, which was higher than (9.81±0.95) mg/L (t=39.784, P=0.000) and lower than 1.00±0.09 (t=13.021, P=0.000) in HCT116 cells. Based on HCT116/L-OHP cells, HCT116/L-OHPcells were established successfully, with relative miR-145 expression of 10.01±1.05, which was higher than 1.06±0.14 in HCT116/L-OHPand 1.00±0.16 in HCT116/L-OHP (F=161.797, P=0.000). GPR98 was identified to be the target gene of miR-145. The relative mRNA and protein expressions of GPR98 in HCT116/L-OHPcells were 8.48±0.46 and 1.71±0.09, respectively, which were higher than those in HCT116/L-OHP(mRNA: 3.65±0.40, protein: 1.21±0.10) and HCT116/L-OHP (mRNA: 3.49±0.35, protein: 1.22±0.08; all P<0.05). The A value was 1.31±0.10, and the relative protein expressions of P-gp and MRP1 were 1.53±0.18 and 1.49±0.20 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP (A value: 0.82±0.08, relative protein expression: 1.00±0.06 and 1.21±0.13, all P<0.05). The A value was 0.89±0.08, and the relative protein expressions of P-gp and MRP were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHP(A value: 0.20±0.05, relative protein expression: 0.20±0.07, 0.55±0.10, all P<0.05). The relative protein expression of PTEN in HCT116/L-OHPcells was 0.12±0.03, which was lower than 1.25±0.14 in HCT116/L-OHP cells(P<0.05). In addition, relative protein expressions of P-gp and MRP1 were 1.02±0.24 and 1.38±0.25 in HCT116/L-OHPcells, which were higher than those in HCT116/L-OHPcells (0.20±0.07 and 0.55±0.10), while PTEN expression in HCT116/L-OHPcells was lower as compared to HCT116/L-OHPcells (1.41±0.16 vs. 1.98±0.13, P<0.05).</p><p><b>CONCLUSION</b>MiR-145 inhibits drug resistance to L-OHP of HCT116 cells through suppressing the expression of target gene GPR98.</p>
Subject(s)
Humans , ATP Binding Cassette Transporter, Subfamily B , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Cell Line, Tumor , Physiology , Colorectal Neoplasms , Down-Regulation , Genetics , Drug Resistance, Neoplasm , Genetics , Physiology , HCT116 Cells , Physiology , In Vitro Techniques , MicroRNAs , Genetics , Pharmacology , Multidrug Resistance-Associated Proteins , Organoplatinum Compounds , Pharmacology , PTEN Phosphohydrolase , RNA, Messenger , Receptors, G-Protein-Coupled , GeneticsABSTRACT
Objective]This article discussed Professor Xie Jianguo's survival with tumor experience on advanced lung cancer treatment in the last decade. [Methods]To observe Professor Xie Jianguo's survival with tumor experience of advanced lung cancer on the clinical treatment process, and organize related cases, which summarized the unique thoughts of treatment, commonly used empirical prescriptions and demonstrated with typical clinical cases. [Resluts] Professor Xie Jianguo's theoretical guidance on advanced lung cancer treatment, included tumor inhibition, anticancer effect, survival with tumor. Treatment methods, included recruitment of the vital qi, adjusting the internal environment, the phlegm, stasis toxin factors, with rigorous thinking, sophisticated medication. [Conclusion] Professor Xie Jianguo's survival with tumor experience on advanced lung cancer treatment has remarkable significance in guiding clinical treatment.
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Objective To investigate the effects of mechanism of silent information regulator of transcription 1 (SIRT1) in the drug-resistance of colonic cancer.Methods The clinical data of 25 colonic cancer patients with 5-Fu-resistance and 30 colonic cancer patients with chemosensitivity who were admitted to the Henan Tumor Hospital from December 2012 to December 2013 were retrospectively analyzed.The specimens of colonic cancer were collected for study.(1) The protein expression of SIRT1 in patients with drug-resistance or chemotherapeutic sensitivity was tested by immunohistochemical staining.The protein expression of SIRT1 in the HCT116 and HCT1 16/5-FU cells was detected by Western blot.(2)HCT116/5-FU cells were interfered by siRNA and divided into the blank control group (cells untreated),the empty vector group (cells treated by siRNA) and the SIRT1 silence group (cells treated by SIRT1 siRNA).The protein expression of the HCT116/5-FU cells were inhibited by the c-Jun N-terminal kinase (JNK) and then divided into the SP600125 group [cells were treated by JNK signaling pathway inhibitor SP60012 (concentration:30 μmol/L)for 12 hours],the DMSO group [cells were treated by DMSO (cells were treated by 0.1% DMSO for 12 hours] and the control group (cells were treated by cell culture media).(3) Serine in the SIRT1 ser47 was mutated to alanine or aspartic acid,and mutations S47A (S47A group,serine to alanine) and S47D (S47D group,serine to aspartic acid) ; Untransfected HCT116/5-FU cells were in the S47 wild type group,and apCMV-3Tag-3 cells transfected by empty vector were served as negative control; all the HCT116/5-FU cells were interfered by 5-FU (concentration:8 μmol/L) for 12 hours.HTC116 cells and HTC116/5-FU cells were treated by SIRT1 inhibitor resveratrol at concentrations of 0,1,10,50,100 nmol/L and SIRT1 activator niacinamide at concentrations of 0,1,2,3,4,5 ng/L.Cell proliferation was detected by MTF.(4) Cell apoptosis was detected by flow cytometry.(5) The expressions of related genes were detected by real-time PCR.(6)The expressions of related proteins were detected by western blot.The count data were analyzed using the chi-square test.The measurement data with normal distribution were presented as (x) ± s.The comparison among groups were analyzed using the one-way analysis of variance and LSD-t test.The pairwise comparisons were analyzed using the t text.Results (1) The results of immunohistochemical staining were as follows.The positive expressions of SIRT1 in patients with chemotherapeutic sensitivity and drug-resistance were 16.7% (5/30) and 92.0% (23/25),respectively,with significant difference (x2 =30.965,P < 0.05).The relative mRNA and protein expressions of SIRT1 in HCT116/5-FU cells with drug-resistance were 1.870 ± 0.100 and 1.660 ± 0.109,which were significantly higher than 1.000 ± 0.070 and 1.000 ± 0.050 in HCT116/5-FU cells without drug-resistance (t =11.721,8.963,P < 0.05).(2) The results of MTT were as follows.The proliferation rates of HCT116/5-FU cells treated by resveratrol at concentrations of 0,1,10,50 nmol/L were 100% ±12%,105%± 14%,129% ± 10% and 144% ± 17%,which were significantly higher than 41% ± 10%,49% ±11%,74% ± 16% and 105% ± 17% of HCT116 cells which were treated by reseratrol at the same contrations (t =8.226,-7.236,6.673,3.510,P <0.05).The proliferation rates of HCT116/5-FU cell treated by niacinamide at concentrations of 0,1,2 ng/L were 87% ± 12%,78% ± 12%,69% ± 11%,which were significantly higher than 36% ± 6%,32%± 5%,30%± 6% of HCT116 cells which were treated by niacinamide at the same concentrations (t =-8.593,-8.006,-7.000,P < 0.05).The proliferation rates of HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 100%± 8%,99% ±9%,37% ± 6%,with significant differences among the 3 groups (F =66.597,P < 0.05),and the proliferation rate of HCT116/5-FU cells in the SIRT1 silence group was significantly lower than that in the blank control group (t =10.113,P <0.05).(3) The results of flow cytometry were as follows.The apoptotic rates of HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 60% ± 5%,36% ± 4%,35% ±4%,with significant differences among the 3 groups (F =36.549,P < 0.05),and the apoptotic rates of HCT1 16/5-FU cells in the SIRT1 silence group were significantly higher than that in the blank control group and the empty vector group (t =-7.215,-7.084,P <0.05).(4)The results of RT-PCR were as follows.The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SIRT1 silence group,the empty vector group and the blank control group were 0.320 ± 0.030,0.990 ± 0.060,1.000 ± 0.090,with significant differences among the 3 groups (F =10.107,P < 0.05),and the relative expression rate of P-gp mRNA in the SIRT1 silence group was significantly lower than that in the blank control group (t =11.463,P < 0.05).The relative expression rates of P-gp mRNA in the HCT116/5-FU cells in the SP600125 group,the DMSO group and the control group were 0.240 ±.0.040,0.990 ± 0.100,1.000 ± 0.070,with significant difference among the 3 groups (F =19.002,P<0.05),and the relative expression rates of P-gp mRNA in the SP600125 group was significantly lower than that in the control group (t =7.301,P <0.05).(5) The results of western blot were as follows.The relative expression rates of p-JNK protein in the HCT116/5-FU cells in the blank control group,the empty vector group and the SIRT1 silence group were 1.000 ± 0.090,1.090 ± 0.020,0.080 ± 0.010,with significant difference among the 3 groups (F =12.130,P < 0.05).The ratios of p-SIRT1-S27/T-SIRT1,p-SIRT1-T530/T-SIRT1,p-SIRT1-S47/T-SIRT1 were 1.158 ±0.140,1.209 ±0.150,3.760 ±0.150 in HCT116 cells treated by 5-FU,and 1.120 ±0.109,1.130 ±0.100,2.160 ±0.110 in HCT116 cells treated by DMSO,with significant differences (F =9.763,10.261,P <0.05).The ratios of p-SIRT1-S47/T-SIRT1 in HCT116 cells treated by 5-FU and DMSO were 3.760 ± 0.150 and 2.160 ± 0.110,which were significantly higher than 0.940 ± 0.040 and 1.121 ± 0.110 in HCT116/5-FU cells (t =14.721,21.335,P < 0.05).(6) The proliferation rates of HCT116/ 5-FU cells in the S47 wild type group,the negative control group,the S47A group and the S47D group were 41%± 31%,39% ± 4%,64% ± 2% and 26% ± 5%,with significant differences among the 4 groups (F =6.371,P < 0.05).Conclusions SIRT1 promotes the proliferation of drug-resistant colonic cancer cells and increases the expression of P-gp via JNK signaling pathway,there by enhances cellular drug resistance.SIRT1 S47 is the critical site for 5-FU-resistance in HCT116/5-FU cells.
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<p><b>OBJECTIVE</b>To investigate the role of death associated protein kinase(DAPK) in colon cancer drug-resistance.</p><p><b>METHODS</b>Immunohistochemistry was used to detect DAPK expression in colon carcinoma tissues of 61 cases and adjacent tissues of 32 cases. 5-fluorouracil (5-FU)-induced drug-resistant colon cancer cell lines HCT116/5-FU model was established. DAPK-siRNA was transfected into cells to down-regulate the DAPK gene expression (DAPK-siRNA grouyp), FAM-siRNA was transfected as control group, and DAPK over-expression plasmid vectors were constructed to up-regulate the DAPK gene expression(DAPK over-expression group). Real-time quantitative PCR and Western blotting were used to examine the mRNA and protein expression levels of DAPK, multidrug resistance protein (MRP) and P- glycoprotein (P-gp). MTT and flow cytometry were used to detect cell proliferation and apoptosis for cells treated with 5-FU (8 mg/L) and cells without treatment of 5-FU in 3 groups respectively.</p><p><b>RESULTS</b>Positive expression rate of DAPK in colon cancer tissues was significantly lower than that in adjacent normal tissues [18.0% (11/61) vs. 90.6% (29/32), P < 0.05]. Compared with FAM-siRNA group, DAPK mRNA and protein expression levels were significantly lower in DAPK-siRNA group, but significantly higher in DAPK over-expression group (P<0.05). After treatment of 5-FU, cell proliferation was significantly inhibited, but cell apoptosis was significantly increased in DAPK over-expression group compared to FAM-siRNA group (P < 0.05). Cell proliferation and apoptosis were not significantly different between DAPK siRNA and FAM-siRNA groups (all P < 0.05). Compared with FAM-siRNA group, DAPK over-expression could significantly reduce the mRNA and protein levels of MRP and P-gp, whereas DAPK siRNA had no obvious such effects.</p><p><b>CONCLUSION</b>DAPK can inhibit the proliferation and promote the apoptosis in drug-resistant colon cancer cells, and it probably enhances the sensitivity of cancer cells to drugs by down-regulating the mRNA and protein levels of MRP and P-gp.</p>
Subject(s)
Humans , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Antineoplastic Agents , Apoptosis , Cell Proliferation , Colorectal Neoplasms , Drug Therapy , Death-Associated Protein Kinases , Metabolism , Drug Resistance, Neoplasm , Fluorouracil , Genetic Vectors , HCT116 Cells , RNA, Messenger , RNA, Small Interfering , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To investigate the association of the expressions of angiopoietin-2 (Ang-2), vascular endothelial growth factor (VEGF) in colorectal cancer tissues with Dukes' clinicopathological features.</p><p><b>METHODS</b>Ang-2 and Tie-2 mRNA expressions were detected in colorectal cancer tissues, adjacent tissues, and normal tissues by real time-PCR. Quantikine immunoassays were used to measure the protein expressions of Ang-2 and VEGF in the tissues and serum samples.</p><p><b>RESULTS</b>Ang-2 and Tie-2 levels were significantly higher in the serum of the patients than in the normal tissues (P<0.05), and their expressions were strongly correlated (r=0.879, P=0.000). Tumor tissue Ang-2 and VEGF levels were significantly higher than their levels in the adjacent and normal tissues (P<0.05). In colorectal cancer patients, the peripheral blood level of Ang-2 was significantly higher than that in healthy control subjects, and comparable with that in mesenteric blood (P>0.05). In Dukes' stage C and D patients, serum Ang-2 and VEGF levels were significantly higher than those in patients in Dukes' stage A and B (P<0.05).</p><p><b>CONCLUSION</b>Ang-2 and VEGF over expressions may play an important role in the occurrence and progression of colorectal cancer.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Angiopoietin-2 , Blood , Metabolism , Case-Control Studies , Colorectal Neoplasms , Metabolism , Pathology , Gene Expression Regulation, Neoplastic , Neovascularization, Pathologic , Vascular Endothelial Growth Factor A , Blood , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To compare the expression patterns of cytokeratin 7 (CK7) and CK20 in the Barrett's esophagus and gastric cardia intestinal metaplasia.</p><p><b>METHODS</b>Endoscopic biopsy specimens from 19 patients with long segment Barrett's esophagus, 36 with short segment Barrett's esophagus, and 20 with histological evidence of gastric cardia intestinal metaplasia were immunostained for CK7 and CK20. The immunohistochemical data were analyzed in relation with the clinicopathological data of the patients including age, hiatal hernia, and Helicobacter pylori status.</p><p><b>RESULTS</b>The Barrett's pattern of CK7/20 expressions was found in all the 19 patients with long segment Barrett's esophagus, in 31 of the 36 (82%) patients with short segment Barrett's esophagus, and in 2 of the 20 (10%) patients with gastric cardia intestinal metaplasia. Patients with short segment Barrett's esophagus who had a Barrett's CK7/20 pattern showed similar clinicopathological findings to those with long segment Barrett's esophagus, while in cases of short segment Barrett's esophagus where no Barrett's CK7/20 pattern was found, the clinicopathological features were similar to those of gastric cardia intestinal metaplasia cases.</p><p><b>CONCLUSION</b>A Barrett's CK7/20 expression pattern is an objective marker of Barrett's mucosa. CK7 and CK20 reactivity patterns in routine endoscopic biopsy samples can reliably identify the location of intestinal metaplasia in the esophagus and stomach.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Barrett Esophagus , Diagnosis , Metabolism , Pathology , Biomarkers , Metabolism , Cardia , Metabolism , Pathology , Keratin-20 , Metabolism , Keratin-7 , Metabolism , Reagent Kits, DiagnosticABSTRACT
Objective To investigate the prognositic factors of small intestine stromal tumors after radical resection.Methods The clinicopathological data of 41 patients with small intestine stromal tumors admitted between January 2005 and December 2010 in Henan Tumor Hospital were analyzed restrospectively.Kaplan-Meier survival rate and COX regression were used to evaluate the prognostic factors.Results There were 22 males and 19 females.The age ranged from 22 to 78 years old (median,55years).Location of tumor included duodenum (n =12),jejunum and ileum (n =29).The 3-year survival rate was 22% in those 16 cases who reported preoperative gastrointestinal bleeding and 65% in those without GIT bleeding,the difference was statistically significant (P =0.0012).COX model showed that tumor size,the tumor location,recurrence and metastasis were independent risk factors associated with the prognosis in small intestine stromal patients (P < 0.05).Conclusions The most common clinical presentation of these tumors was gastrointestinal bleeding.The tumor location,recurrence and metastasis and gastrointestinal bleeding was independent risk factors associated with the prognosis of small intestine stromal tumor patients.
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Objective To observe the clinical effects of Xie's Feiai No.1 formula on patients with advanced non-small cell lung cancer (NSCLC) and its influence on body immune system, VEGF (blood vessel endothelia growth factor) and CYFRA21-1 (keratoprotein 21-1). Methods 650 cases of advanced NSCLC were randomized into a treatment group and chemotherapy group, with 350 cases and 300 cases in each group respectively. The treatment group was administrated with Xie's Feiai No.1 formula, while the chemotherapy group was treated with chemotherapy ofGP plan/TP plan. Both groups were treated for 2 months. Results The short-term effective rate was 56.57% in the treatment group, which was superior to 44.33% (P<0.01) in the chemotherapy group; Steady rate KPS score improvement was 85.14% in the treatment group, which was also higher than 27.00% (P<0.01) in the chemotherapy group; besides the levels of total T cell, adjuvant T cell and NK cell in the treatment group were higher than the chemotherapy group, while the levels of Ts cell, VEGF and CYFRA21-1 int the treatment group were lower than the chemotherapy group. Long-term efficacy observation showed that the survival rate of 117 cases with advanced NSCLC was 83.59% in one year and 46.27% in three years in the treatment group, both significantly higher than those in the chemotherapy group (P<0.01).Conclusion Xie's Feiai No.l formula can increase NSCLC patients' survival time, improve quality of life, strengthen immunological function and restrain tumor cells' activities.
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Objective To investigate application of modified abdominal closure technique by an all layer in ventro-pelvic part operation and evaluate its value and significance. Methods 3200 cases with ventre-pelvic part operation between May 2002 and Aug 2007, were subjected to single layer closure with non absorbable suture material. The clinic data and some results of follow-up were retrospectively analyzed. Results Operative incisions of 1780 (55.6%) cases were in epigastric zone and their rate of primary healing was 98.5%, others (44.3%) in hypogastric zone (including pelvic cavity) and rate of primary healing was 98.2% (P>0.05). Rate of primary healing in older age-group was 97.9% and control group 98.8%, and primary healing of group diabetes 97.4%, control group 98.2% (P > 0.05). Average time of abdmenal closure was only 11±4 min. Primary complications included dehiscence of wound (0.5%), infection (1.4%) and incisional hernia (0.2%). Follow-up (66%) was performed at 30 days, 3 and 6 months, and at 1, 2 and 3 years. Conclusion It is concluded that closure of an abdominal incision can be effected by a multifilament interrupted absorbable sutures without an increased risk of wound dehiscence or incisional hernia, meanwhile economic and fast. It is the optimal method of abdominal closure and can be generalized.
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Objective To observe the recent effect and influence of Lung Cancer Fang No.1 on immunologic function and serum vessel endothelia growth factor (VEGF), keratoprotein 21-1 (CYFRA21-1) in non-small cell lung cancer patients (NSCLC). Methods One hundred non-small cell lung cancer patients were randomized into 52 cases of treatment group on Lung Cancer Fang No.1 and 48 cases of chemotherapy group. The treatment group was treated by Lung Cancer Fang No.1, and the chemotherapy group by GP or TP programme for 2 treatment courses. Immune function indexes, serum VEGF and CYFRA21-1 were determined before and after treatment. Results Efficacy for the treatment group recently was 76.92%, better than 43.75% of the chemotherapy group (P
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Objective To investigate the characteristics of pulmonary infection and susceptible factors following orthotopic liver transplantation (OLT). Methods Clinical data of 128 patients who underwent OLT from Feb. 1999 to Dec. 2004 were studied retrospectively in order to analyze primary pathogens, infectious time and susceptible factors.Results Forty-eight ( 37.5 %) of 128 patients had pulmonary infections and 27 ( 56.3 %) of them developed within postoperative 7 days. Thirty-four ( 70.8 %) cases suffered from mixed infection and 6 ( 12.5 %) died in the hospital after OLT. The primary pathogenic germs included Pseudomonas aeruginosa, Acinetobacter baumannii/haenolyticus, Golden staphylococcus, Aspergilosis and so on.Conclusion Pulmonary infection can be caused by various pathogens and associated with patients' constitution, mechanical ventilation, immunosuppressive drugs and so on.
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Objective To introduce the birth and development of model of end-stage liver disease(MELD) and evaluate its effect on liver transplantation(LT) as a new scoring system.Methods Literatures of MELD applied in LT were analyzed retrospectively.Results MELD scoring system was used for predicting the prognosis of patients with end-stage liver disease and the death risk of candidates on waiting LT extensively and the order of organ sharing was determined by its predicable results.Conclusion MELD has been had a successful initial implementation for predicting the short-term survival probability and mortality in patients with end-stage liver disease,and meeting the goal of providing a system of allocation that emphasizes the urgency of the candidate while diminishing the reliance on waiting time,which has been proven to be a powerful tool for auditing the liver allocation system.
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Objective To explore the status and perioperative management of liver transplantation in treatment of portal hypertension. Methods Clinical data of 56 patients with portal hypertension who underwent (orthotropic) liver transplantation (OLT) from February 2000 to April 2004 were studied retrospectively.(Incidence) of complications,and in-hospital mortality and survival rate were analyzed. Platelet count after OLT was measured and liver blood flow was monitored by Doppler. Results Among the 56 OLT patients, 6 cases(10.7%) underwent simultaneous splenectomy. Incidence of complications was 40.3%,and in-hospital mortality and 1-,2-,and 3- year survival rate after OLT were 12.5% and 87.46%,85.19% and 81.58% respectively. Platelet count reached a nadir at post-transplant day 3. Conclusions OLT is an (effective) method for radical treatment of portal hypertension. Perioperative management is of vital importance for success of the operation and patient′s prognosis.