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Objective@#To establish the culture technique for culturing γδ T cells in vitro and evaluate the basic characteristics, security and anti-tumor effect of the cultured γδ T cells.@*Methods@#Phytohemagglutinin, zoledronic acid, interleukin-2 and interleukin -7 were used to induce the abundant expansion of peripheral blood mononuclear cells in vitro. Flow cytometry assay, in vitro killing assay and mouse model of human lung cancer were also adopted to assess the characteristics and the anti-tumor effect of cultured γδ T cells. Additionally, the contamination of exogenous agents and the acute toxicity of γδ T cells were determined.@*Results@#After culturing 14-16 days in vitro, the total number of γδ T cells was more than 1.0×1010. Among these γδ T cells, CD3+ γδ TCR+ cells accounted for more than 90%. None of contaminations of bacteria, fungi, mycoplasma and virus were observed. At effect target ratio (E/T ratio) of 50/1, killing efficiency of γδ T cells cultured in vitro to SK-MES-1, Ho8910, A549 and K562 reached more than 65%. In vivo experiments showed that the tumor volume of γδ T-treated mice was (828.99±61.05) mm3, significantly lower than (1 723.51±84.30) mm3 of the control mice (P<0.05). Meanwhile, no acute toxicity effect was observed in γδ T cells treated mice.@*Conclusion@#The number, purity and activity of γδT cells cultured in our institute can reach the requirement of clinical application, and the γδT cells also display strong cytotoxic activity against tumor cells such as lung cancer, ovarian cancer and leukemia.
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Objective To explore MRI manifestations and characteristics of primary central nervous system lymphoma in order to improve diagnosis and differential diagnosis. Methods A retrospective analysis was conducted on MRI manifestations of 11 cases of primary central nervous system lymphoma confirmed by surgery, pathology and needle biopsy. Results Ten cases of solitary lymphoma and 1 case of multiple lymphoma were observed. The lymphoma was located in the frontal lobe for 3 cases, the temporal lobe for 3 cases, the parietal lobe for 2 cases, the periventricular area for 2 cases, and the basal ganglia area for 1 case. All of the 11 cases demonstrated obvious enhancement. 10 cases had irregular tumor shape, 9 cases had homogenous enhancement and 2 cases had cystic change or lesion. Cusp sign, dent depression sign and specific feature of butterfly sign were observed in 8 cases. Conclusion Primary central nervous system lymphoma should be considered when there is homogenous signal, irregular shape, obvious enhancement and cusp sign, dent depression sign and butterfly sign.
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<p><b>OBJECTIVE</b>To introduce different surgical treatment for gyncomastia at different grades.</p><p><b>METHODS</b>37 cases with gynecomastia were divided into three grades as: grade I with fat as main tissue, grade II with proliferated fibro-gland as main tissue, grade III with big and ptosis breasts and sagging skin. Different surgical methods were chosen according to the different grades of gyncomastia. These include liposuction, subareolar fibroglandular tissue removing, combined technique of the two methods, and breasts resection with free transplantation of nipple-areola complex.</p><p><b>RESULTS</b>All patients were satisfied for the appearance of post-operative flat male chest. Complications, such as scar, numbness of nipple and areola were acceptable for them.</p><p><b>CONCLUSIONS</b>Different surgical methods should be chosen for the gynecomastia at different grades. It can improve both the physical and psychological problems for patients.</p>
Subject(s)
Adolescent , Humans , Male , Gynecomastia , Classification , General Surgery , Lipectomy , Mammaplasty , Methods , Nipples , Transplantation , Retrospective StudiesABSTRACT
Objective To investigate the effects of testosterone (T) replacement therapy (TRT) on carotid artery intima-media thickness (IMT) in middle aged and elderly male patients.Methods A total of 80 middle-aged and elderly male patients with testosterone deficiency and increased carotid artery IMT were selected and randomly divided into two groups:the treatment group (n=38,treated with testosterone for 1 year) and the control group (n=42,without any treatment).The serum T level,IMT and prostate-specific antigen (PSA) before and after treatment were determined.The correlation between the testosterone level and carotid artery IMT was analyzed.Results There were no significant differences in the serum T level and IMT between the control group and the treatment group before treatment [(10.39 ± 1.44) nmol/L vs.(10.88 ± 1.87) nmol/L,(1.25 ±0.11) mm vs.(1.24±0.13) mm,t=1.32,-0.26,P=0.191,0.794].Compared with pretreatment,the serum T level was significantly increased and the IMT was significantly decreased in the treatment group afterTRT [(10.88±1.87) nmol/L vs.(22.83±1.56) nmol/L,(1.24±0.13) mmvs.(1.18±0.16) mm,t=-29.14,2.55,P=0.000,0.015],while no significant differences in the serum T level and IMT were found in the control group before and after treatment [(10.39± 1.44)nmol/L vs.(9.99±1.72) nmol/L,(1.25±0.11) mm vs.(1.27±0.11) mm,t=1.24,-1.00,P =0.219,0.323].Linear correlation analysis showed that the serum T level was negatively correlated with IMT (r-0.605,P=0.000) and multiple regression analysis showed that the T level was an independent factor for IMT.Conclusions Testosterone replacement therapy is an effective treatment to alleviate IMT in middle-aged and elderly male patients,which may play an important role in preventing cardiovascular diseases in middle-aged and elderly male patients.
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<p><b>OBJECTIVE</b>To discuss the tumorigenicity of immortalized endothelial cells differentiated from embryonic stem cells.</p><p><b>METHODS</b>The embryoid bodies (EB) formed in vitro from embryonic stem cells, were induced to differentiate into many "round cells" (the precursor of endothelial cells). These "round cells" later formed the vascular tube-like structures. To immortalize these cells, human telomerase reverse transcriptase (hTERT) cDNA was transfected into "round cells" by lipofectin, RT-PCR and immunocytochemistry were used to evaluate the immortalized cells. And the tumorigenicity of these cells were evaluated by being injected into nude mice subcutaneously.</p><p><b>RESULTS</b>95% of these transfected cells expressed Flk-1, CD34 and vWF, and could proliferate in large quantity in vitro (cell number was doubled in 2 days, and increased 12 times in 3 days), and were able to form tubular structures.</p><p><b>CONCLUSIONS</b>These results suggest that hTERT cDNA transfection can immortalize induced endothelial cells and tumorigenicity is found after immortalized cells are injected into nude mice subcutaneously.</p>
Subject(s)
Animals , Mice , Carcinogenicity Tests , Cell Differentiation , Cells, Cultured , Embryonic Stem Cells , Cell Biology , Endothelial Cells , Cell Biology , Endothelium, Vascular , Cell Biology , Mice, Inbred Strains , Mice, Nude , Telomerase , Genetics , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To study the effect of genistein (Gen) on MAPK signal pathway in the CIA rat fibroblast-like synoviocytes (FLS).</p><p><b>METHODS</b>The rat model of collagen-induced arthritis (CIA) was established. The cultured FLS of CIA rats were divided using randomized method. The effects of Gen (at the concentration of 50, 100, and 200 micromol/L, respectively) on the proliferation of FLS in CIA rats using methyl thiazolyl tetrazolium (MTT) assay. Effects of Gen (at the concentration of 50, 100, and 200 pmol/L, respectively) on the expressions of extracellular signal-regulated kinase (ERK) and phosphorylated extracellular signal-regulated kinase (p-ERK) in the FLS of CIA rats were detected.</p><p><b>RESULTS</b>Gen could inhibit the proliferation of FLS in CIA rats. The FLS proliferation in the high dose Gen group at 72 h was only 1.10+/-0.04, significantly lower than that in the model group (2.12+/-0.03, P<0.01). Besides, after Gen's action on FLS, the expression of p-ERK was down-regulated. It was only 0.34+/-0.02 in the high dose Gen group, significantly lower than that in the model group (2.68+/-0.14, P<0.01). There was no change in the expression of ERK (P>0.05).</p><p><b>CONCLUSIONS</b>Gen could inhibit the proliferation of FLS in CIA rats. Its mechanism of action was mainly correlated to down-regulating the tyrosine kinase of MAPK signal transduction pathway and inhibiting phosphorylation of ERK.</p>
Subject(s)
Animals , Female , Rats , Arthritis, Experimental , Metabolism , Cells, Cultured , Extracellular Signal-Regulated MAP Kinases , Metabolism , Genistein , Pharmacology , MAP Kinase Signaling System , Rats, Sprague-Dawley , Synovial Membrane , Cell Biology , MetabolismABSTRACT
<p><b>BACKGROUND</b>Tissue inhibitor of metalloproteinase (TIMP)-1 is a multifunctional protein. The aim of the study was to examine the feasibility of using a combination of adenovirus-mediated gene delivery of TIMP-1 plus endostatin and cell transplantation techniques to treat tumor growth and metastasis in mouse melanoma.</p><p><b>METHODS</b>A enzyme-linked immunosorbent assay (ELISA) was used to detect the level of TIMP-1 and endostatin in vitro and in vivo. A tumor bearing mouse model and an experimental lung metastasis model in animal experiments were used to explore the therapeutic effect of in vivo production of human TIMP-1 and endostatin after the implantation of primary fibroblasts infected with the indicated adenovirus into tumor-bearing mice and a cytochemical method was used to observe histopathological changes of the tumor. An experimental lung metastasis model was established by injecting B16BL6 cells into the tail vein of mice and adenovirus-infected primary fibroblasts were subcutaneously implanted into the mice 24 hours later. Twenty-one days after tumor cell injection, mice were sacrificed to examine the effect on nodules visible as black forms on the surface of the lungs in B16BL6 cells.</p><p><b>RESULTS</b>TIMP-1 and endostatin were secreted into the supernatants of cultures of Ad-TIMP-1 and Ad-End-infected mouse primary fibroblasts. We also observed that implantation of fibroblasts infected with Ad-TIMP-1 alone, Ad-End alone, or Ad-TIMP-1 plus Ad-End resulted in detectable blood levels which may clearly inhibit the tumor growth and metastasis in a murine melanoma model.</p><p><b>CONCLUSION</b>These results suggest the high capacity of transfection for the delivery of TIMP-1 or endostatin gene constructs into primary fibroblasts, and demonstrate that the implantation of TIMP-1 and endostatin producing fibroblasts at a site in vivo where direct secretion of TIMP-1 and endostatin into the blood is possible represented a promising approach for the development of cancer therapy.</p>
Subject(s)
Animals , Humans , Mice , Adenoviridae , Genetics , Cell Line , Cell Line, Tumor , Endostatins , Blood , Genetics , Metabolism , Enzyme-Linked Immunosorbent Assay , Fibroblasts , Cell Biology , Metabolism , Melanoma , Therapeutics , Mice, Inbred C57BL , Tissue Inhibitor of Metalloproteinase-1 , Blood , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect and safety of low-dose aspirin for primary prevention of cardiovascular events.</p><p><b>METHODS</b>We searched for randomized controlled trials (RCT) in the following electronic databases: MEDLINE, EMbase, the Cochrane Library (Issue 3, 2008), CBM, CNKI. Quality assessment and data extraction were conducted by two reviewers independently. All data were analyzed using Review Manager 4.2.</p><p><b>RESULTS</b>Six studies (TPT, HOT, PPP, WHS, POPADAD, J-PAD) involving a total of 72,466 participants met the inclusion criteria. Meta-analysis results showed that: (1) Compared with placebo, the incidences of total cardiovascular events (RR = 0.85, 95% CI: 0.80-0.92), stroke (RR = 0.87, 95% CI: 0.77-0.98), nonfatal stroke (RR = 0.81, 95% CI: 0.70-0.95) and transient ischemic attack (RR = 0.76, 95% CI: 0.64-0.90) were significantly lower in low-dose aspirin group than those in placebo control group (all P < 0.05). (2) Nonfatal myocardial infarction (RR = 0.89, 95% CI: 0.77-1.02), death from cardiovascular causes (RR = 0.98, 95% CI: 0.86-1.13) and death from any cause (RR = 0.95, 95% CI: 0.88-1.02) were similar between the 2 groups (all P > 0.05). (3) The risk of coronary heart disease was reduced in low-dose aspirin group in the elderly (RR = 0.81, 95% CI: 0.70-0.94, P < 0.05). (4) The risk of bleeding was higher in low aspirin group compared to placebo group (RR = 1.15, 95% CI: 1.12-1.18, P < 0.01).</p><p><b>CONCLUSIONS</b>Low-dose aspirin use could reduce the incidences of total cardiovascular events, stroke, nonfatal stroke and transient ischemic attack but increase the risk of bleeding, the incidence of nonfatal myocardial infarction, death from cardiovascular causes and death from any cause was not affected by low-dose aspirin use. Low-dose aspirin use was also significantly reduced the risk of coronary heart disease in the elderly.</p>
Subject(s)
Humans , Aspirin , Therapeutic Uses , Cardiovascular Diseases , Drug Therapy , Platelet Aggregation Inhibitors , Therapeutic Uses , Primary Prevention , Randomized Controlled Trials as Topic , Treatment OutcomeABSTRACT
<p><b>BACKGROUND AND OBJECTIVE</b>Transcriptional silencing induced by CpG island methylation is believed to be one of the important mechanisms of carcinogenesis. Checkpoint with fork head-associated and ring finger (CHFR) governs the transition from prophase to prometaphase in response to mitotic stress. This study was to analyze the relationship between the methylation of CHFR gene and the clinicopathologic features of gastric cancer, and the difference of results between methylation-specific polymerase chain reaction (MSP) and combined bisulfite restriction analysis (COBRA) in detecting aberrant methylation of CHFR gene in gastric cancer.</p><p><b>METHODS</b>Both MSP and COBRA methods were used to detect the promoter methylation of CHFR gene in gastric cancer specimens from 64 patients. The relationship between methylation status of CHFR gene and the clinicopathologic features of gastric cancer were analyzed using SPSS16.0.</p><p><b>RESULTS</b>The methylation rates of CHFR gene promoter were significantly higher in gastric cancer samples than in the corresponding paracancer normal gastric mucosa by MSP (51.6% vs. 18.8%, P < 0.001). However, there was no significant correlation between methylation status of CHFR gene and the clinicopathologic parameters of gastric cancer, including age, gender, tumor size, clinical stage, Borrman type, tumor invasion depth, differentiation, and lymph node metastasis (P > 0.05). Aberrant methylation of the CHFR gene was detected in 27 (42.2%) of the 64 specimens of gastric cancer using COBRA, which did not significantly differ from that using MSP (P > 0.05).</p><p><b>CONCLUSIONS</b>Aberrant methylation of the CHFR gene is a frequent event in the carcinogenesis of gastric cancer. Detecting the methylation of CHFR gene in gastric mucosa may conduce to the diagnosis of gastric cancer. No difference was found between MSP and COBRA in detecting promoter methylation of CHFR gene in gastric cancer.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Cell Cycle Proteins , Genetics , DNA Methylation , DNA, Neoplasm , Genetics , Lymphatic Metastasis , Neoplasm Invasiveness , Neoplasm Proteins , Genetics , Neoplasm Staging , Poly-ADP-Ribose Binding Proteins , Polymerase Chain Reaction , Methods , Promoter Regions, Genetic , Genetics , Stomach Neoplasms , Genetics , Pathology , Sulfites , Chemistry , Ubiquitin-Protein LigasesABSTRACT
Objective To evaluate the effectivity and safety of dual antiplatelet therapy with clopidogrel and aspirin in patients with ST-segment elevation acute yocardial infarction(AMI).Methods We searched for randomized controlled trials(RCTs)and quasi-RCTs in the following electronic databases:PubMed,EMBASE,The Cochrane Library(Issue 3,2007),CBM,CNKI,VIP and Wanfang.Quality assessment and data extraction were conducted by two reviewers independently.Disagreement were resolved through discussion.All data were analyzed by using Review Manager 4.2. Results Ten studies involving a total of 52 433 participants met the inclusion criteria.Metaanalysis results showed that:(1)Compared with aspirin alone,the incidence rates of death caused by any reason(RR=0.91,95% CI:0.85~0.97),recurrent myocardial infarction(RR=0.80,95% CI:0.72~0.89),stroke(RR=0.81,95% CI:0.68~0.96),post-infarction angina(RR=0.35,95% CI:0.19~0.66),incoronary thrombus(RR=0.73,95% CI:0.64~0.83)and the combined endpoint events of death,reinfarction or stroke(RR=0.89,95% CI:0.84~0.95)could be reduced by clopidogrel and aspirin.(2)There were no significant differences in ameliorating the cardiac function and increasing TIMI blood flow of infarct-related artery between the two groups RR=0.97,95% CI:0.92~1.03;RR=1.14,95% CI:1.00~1.30;both P>0.05.(3)There was no significant difference in bleeding between the tWO groups(RR=1.11,95% CI:0.92~1.34). Conclusions Compared with aspirin alone,clopidogrel plus aspirin has good effects on reducing the incidence rates of death caused by any reason,recurrent myocardial infarction,stroke,post-infarction angina,incoronary thrombus and the combined endpoint events of death,reinfarction or stroke in patients with ST-segment elevation AMI,and it has the same efficacy in ameliorating the cardiac function,increasing TIMI blood flow of infarct-related artery and bleeding.
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Objective: To evaluate the effect of hypoxia on migration, invasion and adhesion to endothelial cells of human pulmonary adenocarcinoma A549 cells. Methods: Wound-healing and Transwell invasion assays were performed to study the effect of hypoxia on migration and invasion of A549 cells. Cell adhesion test was used to detect the adhesion of A549 cells to a monolayer of human umbilical vein endothelial cells (HUVECs). Immunofluorescence assay was used to evaluate the effect of hypoxia on distribution of E-cadherin, β-catenin, and F-actin. The luciferase reporter gene assay was performed to detect the transcription of hypoxia-inducible factor-1 (HIF-1) alpha. Results: Hypoxia promotes A549 cell migration, invasion, and adhesion to endothelial cells, and modulated the distribution of E-cadherin and β-catenin and rearrangement of actin cytoskeletal protein, and up-regulated HIF-1-dependent reporter gene expression in A549 cells. Conclusion: Hypoxia promoted A549 cell migration, invasion, and adhesion to endothelial cells by upregulating HIF-1-dependent gene expression, subsequently affecting the redistribution of E-cadherin and β-catenin and rearrangement of F-actin cytoskeletal protein.
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This study was aimed to investigate the effect of genistein (gen) on the expression of hypoxia inducible factor-1alpha (HIF-1alpha) induced by cobalt chloride (CoCl(2)) in human leukemia cell line K562. The hypoxia condition was simulated by CoCl(2); the dose- and time-effect groups were prepared as follows: the former were exposed to 0, 50, 100 and 150 micromol/L of CoCl(2) for 72 hours, the latter were detected at 0, 24, 48 and 72 hours while treated with CoCl(2) 100 micromol/L. The gen-treated samples were divided into five groups: (1) normal control; (2) CoCl(2) 150 micromol/L; (3) CoCl(2) 150 micromol/L + gen 50 micromol/L; (4) CoCl(2) 150 micromol/L + gen 100 micromol/L; (5) CoCl(2) 150 micromol/L + gen 200 micromol/L. The HIF-1alpha mRNA and protein were detected by RT-PCR and Western blot respectively. The results indicated that the expression of HIF-1alpha protein in K562 cells induced by CoCl(2) increased in dose-and time-dependent manner (p<0.01), while the expression of HIF-1alpha mRNA in K562 cell remained the similar level (p>0.05). Gen significantly inhibited the expression of HIF-1alpha protein induced by CoCl(2) in dose-dependent manner (p<0.01) while the HIF-1alpha mRNA expression was not affected by treatment of gen (p>0.05). It is concluded that CoCl(2) dose- and time-dependently induced the HIF-1alpha protein expression; HIF-1alpha mRNA was constantly expressed regardless of normoxic conditions or in the presence of cobalt ion under normoxic conditions. Gen can inhibit HIF-1alpha expression in K562 cell induced by CoCl(2) at level of protein, but not mRNA.
Subject(s)
Humans , Cobalt , Pharmacology , Down-Regulation , Genistein , Pharmacology , Hypoxia-Inducible Factor 1, alpha Subunit , Genetics , Metabolism , K562 Cells , RNA, Messenger , Genetics , MetabolismABSTRACT
Objective To investigate the effect of chemotherapy combined with amino acid on quality of life(QOL)in elderly patients with non-small cell lung cancer(NSCLC). Methods Seventy-four elderly patients with NSCLC were divided randomly into experimental group and control group.The same NP(cisplatin+vinorelbine)chemotherapy was carried out in all the 2 groups for 3 cycles.Except of chemotherapy,experimental group were treated with amino acid 500 ml/d in the same time,while control group recieved chemotherapy only.After 3 monthes,the QOL was analyzed using Chinese Version of European Organization for Researeh and Treatment of Cancer(EORTC)core questionnaire(QLQ-C30)and specific lung cancer module QLQ-LC13,and therapeutic effectiveness was evaluated according to WHO standard as well. Results After chemotherapy,the body function,mood function,social function were better in experimental group than in control group(all P<0.05),the effective rate was 87.8%,83.8%and 77.0%in experimental group;77.0%,45.9%and 45.9%in control group.Insomnia(8.1%),suppressed appetite(5.4%),weary(47.3%)were less serious in experimental group than in control group(17.6%,17.6%and 59.5%)(all P<0.05).The primary symptoms were cough,emptysis,thoracalgia and dyspnoea in both 2 groups before chemotherapy.All the symptoms were alleviated after chemotherapy.Some patients have side effects such as tongue pain,alopecie,hand and foot tingle.But the number of patients with tongue pain was less in experimental group(8.3%)than in control group(18.4%).The chemotherapy effect had no difference by the WHO standard. Conclusions The QOL of elderly patients with NSCLC can be improved by chemotherapy combined with amino acid treatment,and the treatment with amino acid 500 ml/d is safety.
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<p><b>OBJECTIVE</b>To explore the effect of arsenic trioxide (As2 O3) on the level of VEGF, VEGFR and the activity of MMP-2, 9 in K562 cells.</p><p><b>METHODS</b>The inhibition ratio of K562 cell was detected by MTT assay, the level of VEGF by Enzyme-linked immunosorbent assay (ELISA), the expression ratio of VEGFR by flow cytometry (FCM), and the activity of MMP-2, 9 by gelatin zymography assay.</p><p><b>RESULTS</b>(1) The IC50 of K562 cells was (2.12 +/- 0.11) micromol/L. Proliferation of K562 cells was significantly inhibited at the concentration of 0.4 - 6.4 micromol/L As2 O3 (P < 0.05). (2) The expression of VEGF was slightly up-regulated by 0.05 micromol/L As2 O3 (P > 0.05) and prominently inhibited by 0.4 micromol/L and 3.2 micromol/L As2 O3 (P < 0.05). As2 O3 had no influence on VEGFR. (3) The activity of MMP-2 and 9 was partly inhibited by 0.05 micromol/L As2 O3 incubated 72 hours and by 0.4, 3.2 micromol/L, As2 O3. With the increase of As2 O3 concentration and the incubation time, the inhibited effect on MMP-2 and 9 was enhanced.</p><p><b>CONCLUSIONS</b>As2 O3 may down-regulate the expression of VEGF and inhibit the activity of MMP-2 and 9.</p>
Subject(s)
Humans , Arsenicals , Pharmacology , Cell Proliferation , K562 Cells , Matrix Metalloproteinase 2 , Metabolism , Matrix Metalloproteinase 9 , Metabolism , Oxides , Pharmacology , Receptors, Vascular Endothelial Growth Factor , Metabolism , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To introduce a modification of Lejour reduction mammaplasty.</p><p><b>METHODS</b>With the upper pedical flap as the base of mammaplasty, the lower part of breast was resected while excess skin was pushed to lateral and formed "L"-shaped scar after it was resected.</p><p><b>RESULTS</b>From October 2005 to April 2006, the modified Lejour reduction mammaplasty was applied to 10 mammahypertrophic patients with 20 breasts in sum. The result of operation was good and only "L"-shape scar was left in the lower lateral part of the breast.</p><p><b>CONCLUSIONS</b>This method is easy to perform and could avoid inverted T scar caused by routine mammaplasty technique. This method is worth introducing widely.</p>
Subject(s)
Adult , Female , Humans , Young Adult , Cicatrix , Mammaplasty , MethodsABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of amino acid parenteral nutritional (PN) support on serum tryptophan and melatonin in non-small cell lung cancer (NSCLC) patients receiving chemotherapy.</p><p><b>METHODS</b>Seventy-two patients with inoperable NSCLC were divided into three groups randomly: control group, 250 ml/d amino acids PN therapy group and 500 ml/d amino acids PN therapy group. The same NP (cisplatin + vinorelbine) chemotherapy was carried out in all the three groups. During three sessions of chemotherapy,amino acids PN therapy was given to the amino acids PN therapy groups. Serum tryptophan and melatonin concentration changes were assessed before and after chemotherapy.</p><p><b>RESULTS</b>After chemotherapy the concentration of MT and Try were much lower than that before chemotherapy in the three group patients (P < 0.05). But the concentration of MT and Try in the PN group patients was higher than that in control group patients. The concentration of MT and Try in the 500 ml/d amino acid parenteral nutritional support group patients were significantly higher than that in the 250 ml/d group patients, the difference was significant (P < 0.05).</p><p><b>CONCLUSION</b>Amino acid parenteral nutritional support is beneficial to improve the lower concentration of serum MT and Try in NSCLC patients receiving chemotherapy, and a more significant effect can be achieved by the 500 ml/d amino acid parenteral nutritional support treatment.</p>
Subject(s)
Aged , Female , Humans , Male , Amino Acids , Therapeutic Uses , Antineoplastic Combined Chemotherapy Protocols , Therapeutic Uses , Carcinoma, Non-Small-Cell Lung , Blood , Drug Therapy , Therapeutics , Cisplatin , Lung Neoplasms , Drug Therapy , Pathology , Therapeutics , Melatonin , Blood , Neoplasm Staging , Parenteral Nutrition , Treatment Outcome , Tryptophan , Blood , VinblastineABSTRACT
<p><b>OBJECTIVE</b>The aim of this review was to assess RNA interference (RNAi) and its possibility as a potential and powerful tool to develop highly specific double-stranded RNA (dsRNA) or small interfering RNA (siRNA) based gene-silencing therapeutics.</p><p><b>DATA SOURCES</b>The data used in this review were obtained from the current RNAi-related research reports.</p><p><b>STUDY SELECTION</b>dsRNA-mediated RNAi has recently emerged as a powerful reverse genetic tool to silence gene expression in multiple organisms. The discovery that synthetic duplexes of 21 nucleotides siRNAs trigger gene-specific silencing in mammalian cells has further expanded the utility of RNAi in to the mammalian system.</p><p><b>DATA EXTRACTION</b>The currently published papers reporting the discovery and mechanism of RNAi phenomena and application of RNAi on gene function in mammalian cells were included.</p><p><b>DATA SYNTHESIS</b>Since the recent development of RNAi technology in the mammalian system, investigators have used RNAi to elucidate gene function, and to develop gene-based therapeutics by delivery exogenous siRNA or siRNA expressing vector. The general and sequence-specific inhibitory effects of RNAi that will be selective, long-term, and systemic to modulate gene targets mentioned in similar reports have caused much concern about its effectiveness in mammals and its eventual use as a therapeutic mordality.</p><p><b>CONCLUSIONS</b>It is certain that the ability of RNAi in mammals to silence specific genes, either when transfected directly as siRNAs or when generated from DNA vectors, will undoubtedly accelerate the study of gene function and might also be used as a potentially useful method to develop highly gene-specific therapeutic methods. It is also expected that RNAi might one day be used to treat human diseases.</p>
Subject(s)
Animals , Humans , Antigens, Neoplasm , Gene Silencing , Genes, abl , Genetic Therapy , Neoplasm Proteins , Genetics , RNA InterferenceABSTRACT
Objective To investigate the effect of recombinant adenovirus mediatied human endostatin (rAD-GFP-ES)on rats with collagen typeⅡinduced arthritis(CIA),and explore the mechanism of inflamma- tion and cytokines inhibition on rats CIA.Methods The rAD-GFP-ES was amplified and purified.The model of rat CIA was induced by intradermal injection of typeⅡcollagen combined with complete Freund's adjuvant(CFA). On the second day after the injection,the therapeutic administration of rAD-GFP-ES(1?10~(11)pfu?kg~(-1)?week~(-1)?4 weeks)were performed to the rats.The mean arthritis index(AI)was scored every week since then.The relative concentrations of ES,IL-I?,TNF-?in sera collected at the fourth week were evaluated by western blotting. Results①The titer of the purified rAD-GFP-ES and rAD-GFP was 6.6?10~(12)pfu/ml and 4.8?10~(12)pfu/ml,re- spectively(A_(260nm)/A_(280nm)>1.3).②The concentration of ES in sera of the group treated with rAD-GFP-ES was 2.4-lold higher compared to the normal group.③The mean arthritis index of the group treated with rAD-GFP- ES was much lower than that of the model group.The administration of rAD-GFP-ES could significantly de- creas the production of IL-1?and TNF-?in sera.Conclusions①The rAD-GFP-ES is efficiently expressed in vivo.②The rAD-GFP-ES has an inhibitory effect on the arthritis index of rat CIA.③IL-1?and TNF-?are involved in the pathogenesis of RA.The rAD-GFP-ES has an inhibitory effect on the expression of IL-1?and TNF-?in rat CIA.