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Objective:To evaluate the cognitive function characteristics in patients with myasthenia gravis(MG).Methods:The cognitive function of 83 MG patients and 39 healthy controls (HC) were evaluated by MMSE, California verbal learning test( CVLT), brief visuospatial memory test revised(BVMT-R), symbol digit modalities test(SDMT), benton judgment of line orientation test(BJLOT), paced auditory serial addition Test(PASAT) and verbal fluency test(VFT). The depression state was assessed by beck depression inventory (BDI). The results were compared between MG and HC groups.The effect of clinical characteristics such as disease type, comorbidities, course of disease, disease severity, and drug treatment on cognitive impairment in MG group was further analysed.Results:The scale scores of MMSE(28(26, 29), 29(28, 30)), CVLT, BVMT-R, SDMT((37.06±12.18), (47.54±14.91)) and PASAT((32.86±10.23), (37.00±8.82)) in MG were significantly lower than those in control group ( P<0.05). There were no statistical difference regarding the scores of BJLOT, VFT and BDI in the two groups( P>0.05). Spearman correlation analysis showed that QMG scores were negatively correlated with SDMT scores( r=-0.234, P<0.05). MG-ADL scores were inversely correlated with total BVMT-R scores of three trials( r=-0.283, P<0.05). Conclusion:Patients with MG suffered from cognitive impairment, mainly in memory, attention, processing speed and visual memory, which supported the hypothesis of CNS involvement in MG.Dysfunction in some cognitive domains may be related to the disease severity.Clinicians need take morce attention to early assessment, developing long-term follow-ups and appropriate intervention.
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Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune demyelinating disease in central nervous system,mainly involving the optic nerves and spinal cord.NMOSD is a relapsing disease with severe residual disability,therefore,prevention of attacks is critical for the preservation of visual and neurologic function.The conventional immunosuppressants,including prednisone,azathioprine,mycophenolate mofetil and methotrexate,can be used to prevent relapse of NMOSD.And immunotherapeutics such as rituximab,tocilizumab and eculizumab are increasingly used in recent years.This review summarizes the current status and the future strategies in treatment of NMOSD based on the progress of NMOSD pathogenesis.
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Objective To explore the clinical features of late-onset neuromyelitis optica spectrum disorders (LON?MOSD). Methods A retrospective analysis was performed to evaluate 61 patients with LONMOSD admitted to our hospital from January 2010 to May 2015. Results (1) The median age at onset was 57 (53, 63) years, male/female was 1∶3.7. Thirty-two patients (52.5%) had transverse myelitis (TM) and 16 patients (26.2%) had optic neuritis (ON) at the disease onset. Fifty-one patients (83.6%) experienced recurrent attacks. Forty patients (65.6%) showed abnormal brain magnetic resonance imag?ing (MRI). Spinal cord MRI showed more frequently present in thoracic regions (39.3%). (2) There were no significant differ?ences in clinical features between AQP-4 seropositive and seronegative groups. (3) By Spearman analysis, it was obvious that EDSS scores at acute phase and remission were positively correlated to AQP-4 antibody levels (rs=0.389, P0.05;rs=0.096, P>0.05). Conclusion LONMOSD patients are more prone to present with TM at onset and have more lesions in thoracic spinal cord and brain. The AQP-4 antibody titres can indicate the severity of disease in acute phase.
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Objective To investigate the mechanism of apoptosis induced by UMI-77 , a novel selective inhibitor of Mcl-1, in gastric cancer MGC-803 cells. Methods MGC-803 cells were treated with UMI-77 in different concen-trations for 24 h, apoptotic rates were determined by Annexin V/PI method using flow cytometry. Mitochondrial membrane potential was determined by JC-1 staining on a flow cytometer. The activation of Caspase-9, Caspase-3 and cleavage of PARP were measured by Western blot analysis. The protein level of Bcl-2, Bcl-XL and Mcl-1 was monitored by Western blot as well. Chemically synthesized Mcl-1 siRNA was transfected into MGC-803 cells using Lipofectamine 2000 Reagent. The efficacy of gene silencing was confirmed by Western blot analysis, and opoptotic rates before and after transfection was measured by flow cytometry using Annexin V/PI staining. Results UMI-77 was effective in induction of apoptosis in gastric cancer MGC-803 cells, apoptotic rates were increased in a dose-de-pendent manner. Mitochondrial membrane potential was collapsed after UMI-77 treatment. Activation of Caspase-9, Caspase-3 and cleavage of PARP occurred at 24 h (P<0. 05). The expression level of Bcl-2 and Bcl-XL were not altered after exposure to UMI-77 , while Mcl-1 was down-regulated after 12 h ( P<0. 05 ) . Transfection with Mcl-1 siRNA successfully decreased the expression level of Mcl-1 in MGC-803 cells ( P<0. 05 ) and blocked apoptosis induced by UMI-77 ( P<0. 05 ) . Conclusion UMI-77 induces apoptosis through activation of the intrinsic path-way in gastric cancer MGC-803 cells, and knocking down Mcl-1 expression abrogates apoptosis by UMI-77.
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Objective To evaluate the patient-controlled paravertebral block (PCPB) in optimizing the cellular immune function when used after radical resection of pulmonary carcinoma performed via video-assisted thoracoscope in patients.Methods Forty-one ASA physical status Ⅰ or Ⅱ patients of both sexes,aged 50-64 yr,with body mass index of 20-25 kg/m2,of TNM staging Ⅰ or Ⅱ,undergoing radical resection of pulmonary carcinoma performed via video-assisted thoracoscope,were randomly divided into 2 groups using a random number table:PCIA group (n =21) and PCPB group (n =20).PCIA solution contained sufentanil 2 μg/kg in 100 ml of normal saline.The PCIA pump was set up to deliver a 2 ml bolus dose with a 15-min lockout interval and background infusion at 2 ml/h.In PCPB group,the patients received paravertebral injection of 0.2％ ropivocaine 5 ml at T5 level on the affected side under ultrasound guidance at the end of operation,and then received PCPB.PCPB solution contained 0.75％ ropivacaine 67 ml in 250 ml of normal saline,and the pump was set up to deliver a 5 ml bolus dose,with a 15-min lockout interval and background infusion at 5 ml/h.VAS score was maintained ≤ 3,and analgesia lasted until 50 h after operation.Before induction of anesthesia (baseline),at end of operation,and at 1,3 and 5 days after operation,peripheral venous blood samples were collected to determine the levels of regulatory T cells,natural killer cells and natural killer T cells (by flow cytometry) and plasma concentrations of interleukin-10 and transforming growth factor-β (by ELISA).Results Compared with group PCIA,the level of regulatory T cells was significantly decreased,the levels of natural killer cells and natural killer T cells were increased,and the plasma concentrations of interleukin-10 and transforming growth factor-β were decreased at 1 and 3 days after operation,and no significant change was found in the rate of cellular immune function decline after operation in group PCPB.Conclusion PCPB provides no significant difference clinically in optimizing the cellular immune function when used after radical resection of pulmonary carcinoma performed via video-assisted thoracoscope in the patients.
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OBJECTIVE:To establish a method for simultaneous determination of ethinylestradiol and norelgestromin in hor-monal patches. METHODS:RP-HPLC method was performed on column of WondaCract ODS-2 with mobile phase of metha-nol-0.5% phosphoric acid(68∶32,V/V)at a flow rate of 1.0 ml/min,the detection wavelength was 220 nm,the detection tempera-ture was 25 ℃,and sample volume was 20 μl. RESULTS:The linear relationship was 0.872-130.8 μg/ml for ethinylestradiol(r=0.999 6) and 0.880-132.0 μg/ml for norelgestromin (r=0.999 7);RSDs of precision,reproducibility and stability tests were no more than 1.03%,average recoveries were resectively 101.50%(RSD=0.99%,n=9) and 101.68%(RSD=0.95%,n=9). CON-CLUSIONS:The established method is simple and accurate,and can be used for the content determination of ethinylestradiol and norelgestromin in hormonal patches.
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We aimed to investigate the expression of inter-leukin 12 [IL-12] family cytokines [IL-12, IL-23, IL-27 and IL-35] and their relevant cytokines [IFN-gamma, IL-4, IL-17A and IL-10] in patients with chronic immune thrombocytopenia [cITP] as well as the effect of high-dose dexamethasone [HD-DXM] treatment on this expression. DXM was administered orally at a dose of 40 mg per day for 4 consecutive days to 38 patients with cITP. We measured the plasma levels of IL-12p70, IL-23, IL-27, IFN-gamma, IL-4 and IL-17A before and after treatment and also in 36 matched healthy controls, by means of FlowCytomix[Tm]technology. The plasma levels of IL-10 and IL-35 were measured by enzyme-linked immunosorbent assay. Significantly higher plasma levels of IL-12p70, IL-23, IL-27, IFN-gamma and IL-17A were observed in cITP patients than in controls [p < 0.01], and after HD-DXM treatment, these levels decreased significantly [p < 0.01]. However, significantly lower plasma levels of IL-4, IL-10 and IL-35 were observed in cITP patients than in controls [p < 0.01]; after the HD-DXM treatment, these levels had increased significantly in the cITP patients [p < 0.01]. Moreover, the cytokine levels of patients who attained a complete response returned to the levels of normal controls [p > 0.05] but were not corrected in the patients who had no response [p <0.01]. The patients with cITP had abnormal expression of the IL-12 family cytokines and their relevant cytokines levels, and HD-DXM treatment corrected the derangement of plasma cytokines. Measuring cytokine levels may help in the clinical assessment of cITP
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Humans , Adult , Middle Aged , Aged , Female , Male , Cytokines , Purpura, Thrombocytopenic, Idiopathic , DexamethasoneABSTRACT
Objective: To investigate whether lipopolysaccharide induced parkin expression and mitophagy in macrophages.Methods:The murine peritoneal primary macrophages were aseptically isolated from Kunming mice and cultured in complete medium.The mitochondrial membrane potential of macrophages was detected by flow cytometry,after the cells were stimulated with 200 ng/ml LPS and labeled mitochondria with JC-1.The parkin mRNA level of macrophages was detected by RT-PCR, protein levels of parkin and autophagic related protein LC3 Ⅱ and LC3 Ⅰ were determined by Western blot.The distribution and co-localization of parkin with LC3 and mitochondria in macrophages were respectively observed by laser scanning confocal microscope, before and after the cells were treated with LPS.Results: Flow cytometry results after JC-1 staining showed that mitochondrial membrane potential in macrophages was declined after stimulation with 200 ng/ml LPS, and continuously decreased with prolonged treatment time.The mRNA levels of parkin were increased slightly within 6 h after LPS stimulation,but parkin proteins were increased significantly within 6 h after LPS stimulation.The results of parkin distribution showed that parkin was evenly distributed in the cytoplasm at normal status, but became the obvious punctate distribution after LPS stimulation in macrophages.Western blot results showed LC3 Ⅱ/LC3 Ⅰ levels were increased after LPS stimulation, indicating the appearance of macrophage autophagy.Confocal microscopy showed that there were co-localization of parkin,LC3 and mitochondrial in macrophages after LPS stimulation.Conclusion:Parkin expression is increased significantly and mediated mitochondrial autophagy in macrophages after LPS stimulation, which is involved in the clearance of damaged mitochondria,thereby playing a role in regulating macrophage inflammatory response.
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Aim To study the effect of simvastatin on the production of reactive oxygen species ( ROS ) and the secretion of interleukin-1 beta ( IL-1β) in oxidized low density lipoprotein ( oxLDL )-induced macropha-ges. Methods After the murine macrophage J774A. 1 was treated with 0,50,100,200 mg·L-1 oxLDL, the contents of aggregated lipid in macrophages were ob-served and determined by oil red O staining. Then, the oxLDL-primed macrophages were treated with 0 . 5 ,1 . 0μmol·L-1 simvastatin, the production of ROS was de-termined by flow cytometry and the expressions of pro-caspase-1 , cleaved caspase-1 and mature IL-1βon pro-tein level were determined by Western blot. Results The oil red O staining results showed that oxLDL could induce obvious lipid aggregation in macrophages, and reached the saturation point with 100 mg·L-1 concen-tration. Flow cytometry results indicated that oxLDL could induce the production of ROS in macrophages, up to 167% ± 0. 47%, and ROS level decreased to 139% ± 0. 97% in a dose-dependent manner after treatment with simvastatin. Western blot indicated that simvastatin could inhibit the expression of cleaved caspase-1 and mature IL-1β in macrophages triggered by oxLDL;compared with oxLDL group, the expression of cleaved caspase-1 and mature IL-1β decreased in simvastatin treated group, and all results had statistical significance ( P<0. 05 ) . Conclusion In the lipid ag-gregation model of macrophages induced by oxLDL, simvastatin can inhibit the production of ROS, caspase-1 activation, and secretion of IL-1β in macrophages.
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Aim To study the sensitivity of human gastric cancer BGC-823 cells to paclitaxel after trans-fection of SHIP2 ( The SH2 domain containing inositol 5-phosphatase 2 ) cDNA. Methods Apoptotic cells were determined by the propidium iodide method using flow cytometry. The levels of protein and mRNA ex-pression were measured by Western blot analysis and qRT-PCR, respectively. pCMV6-SHIP2 plasmid and empty vector were transiently transfected into BGC-823 cells, respectively. Stable cell lines were established after infecting BGC-823 cell with GV112-Puromycin and GV112-Puromycin-Bim( Bcl-2 interacting mediator of cell death) lentivirus particles. pCMV6-SHIP2 plas-mid was transiently transfected into the stable cell lines. Results BGC-823 cells were relatively insensi-tive to paclitaxel compared with SGC-7901 cells. The apoptotic rate was only (25. 6 ± 1. 6)% after the treat-ment with 0 . 3 μmol · L-1 paclitaxel for 48 h in BGC-823 cells. The expression levels of Bim protein and mRNA in BGC-823 cells treated with paclitaxel at dif-ferent time points were not significantly changed. The expression of Bim protein was increased after transfec-tion of pCMV6-SHIP2 plasmid, and the apoptotic rate was up to ( 50. 8 ± 0 . 9 )% in BGC-823 cells treated with paclitaxel for 48h. The expression of Bim protein was significantly inhibited after infecting with GV112-Puromycin-Bim lentivirus particles. The apoptotic rate of infected BGC-823 cells was only ( 27. 6 ± 1. 6 )%after treatment upon paclitaxel for 48h. Conclusion Overexpression of exogenous SHIP2 can increase the expression of Bim, induce apoptosis and enhance sen-sitivity of BGC-823 cells to paclitaxel.
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Aim To investigate the potential involve-ment of caspase-4 in TRAIL ( tumor necrosis factor-re-lated apoptosis-inducing ligand )-induced apoptosis in gastric cancer cells. Methods The effect of treatment with TRAIL /z-LEVD-fmk alone or in combination for 24 h on the apoptotic rate of gastric cancer cells was detected by FCM ( flow cytometry) using propidium io-dide DNA staining. Chemically synthesized three siR-NAs targeting caspase-4 gene were transfected into gas-tric cancer cells by Lipofectamine 2000 Reagent. The efficacy of gene silencing was confirmed by Western blot analysis . The apoptotic rates of gastric cancer cells to TRAIL before and after transfection with caspase-4 siRNA were observed by FCM. The expression level of GRP78 (78-ku glucose-regulated protein) protein was examined by Western blot, the classic endoplasmic re-ticulum stress inducer tunicamycin ( TM) was used as a control. The expression levels of caspase-4 and caspase-3 after TRAIL treatment were also measured by Western blot. Results z-LEVD-fmk decreased TRAIL-induced apoptosis of gastric cancer cells signifi-cantly(P<0. 05). As compared with negative control, the expression level of caspase-4 protein was reduced after transfection, and the apoptotic rate was also de-creased ( P <0. 05 ) . While TM induced marked up-regulation of GRP78 , treatment with TRAIL resulted in, albeit to a lesser extent, increases in GRP78, in-dicative of induction of ER stress by TRAIL. Activa-tion of caspase-4 and caspase-3 occurred early after TRAIL treatment. Conclusion Activation of caspase-4 contributes to TRAIL-induced apoptosis and is asso-ciated with induction of ER stress by TRAIL in gastric cancer cells.
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Objective To investigate the effects of Arctigenin ( ATG ) on concanavalin ( ConA )-stimulated cell proliferation and cytokine secretion in mouse spleen cells, and its possible mechanism. Methods The toxicity of ATG on mouse spleen cells was determined by MTT assay. The inhibition of proliferation was investigated by tritiat-ed thymidine incorporation method. Secreted cytokines (IFN-γand IL-2) were analyzed by ELISA. The associated proteins and phosphorylation levels of mTOR pathway ( mTOR/P70 S6 K/Akt/AMPK/Raptor ) were detected by Western blot. Results ATG had no significant toxicity to mouse spleen cells. ATG significantly inhibited mouse primary spleen cells proliferation induced by ConA. ATG suppressed IL-2 and IFN-γ production of mouse spleen cells in a concentration-dependent manner. ATG remarkably suppressed the phosphorylation of mTOR and P70S6K, and enhanced the phosphorylation of upstream AMPK and Raptor, while the phosphorylation of Akt did not change significantly. Conclusion ATG markedly suppresses the proliferation of mouse spleen stimulated by ConA cells and secretion of IFN-γand IL-2 , which may be correlated to the abilities of enhancing the phosphoryla-tion of AMPK and Raptor, inhibiting the phosphorylation of mTOR and P70S6K.
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Objective To establish a new method for quantitating leukocyte fragments (LFs) in apheresis platelet concentrates (AP-PCs) by using real-time quantitative polymerase chain reaction (RQ-PCR) and flow cytometry(FCM) and discuss the factors influencing LFs concentrations such as storage time, filtration and PLT concentration. Methods 67 qualified donors were selected. Each of them donated one therapeutic dose of AP-PCs. AP-PCs samples were collected as soon as possible and divided into si xfractions. One was analyzed by hematology analyzer. For the Others, DNA was extracted under differen tconditions (filtrated or unfiltrated, before or after centrifugation) at 4 hours, 24 hours, 48 hours, 72 hours, 96 hours after blood draw, respectively. Then the amounts of albumin gene of the AP-PCs and the cell-free DNA in supematant were quantitatively determined using RQ-PCR and the results were calculated into leukocytes equivalent(WBCs/μl). Intact leucocytes were counted by FCM. The concentrations of LFs were calculated by subtracting cell-frce DNA and intact leucocytes from the total DNA amount. Then the differences of LFs concentrations among groups with different storage time were compared and the differences of LFs concentrations between unfihrated and filtrated groups were also compared. After grouping all the AP-PCs according to their PLT concentrations, LFs contents of AP-PCs before filtration among groups were compared. Meanwhile, bivariate correlation analysis between PLT concentrations and LFs contents was carried out. ResultsLFs contents of all the AP-PCs samples were quantitated successfully.The concentrations of LFs in AP-PCs before filtration in 4 hours,24 hours,48 hours,72 hours , 96 houres after blood draw were(31.4±17. 6), (47.5±25.3), (100.7±53.5), (89.5 ±47.2) and (16.1±7.8) WBCs/μl ; After filtration the results were (16. 9±8. 7), (24. 3 ± 12. 2), (83. 1±42. 6), (78.2 ±40. 2) and (13.6 ± 6. 6) WBCs/μl respectively. There were statistically significant differences among groups of different storage time (Fwithin subjects = 472. 756,P < 0.01). The concentrations of LFs kept on increasing within 48 hours after collections, and then decreased gradually. The peaks appeared between 48 hours and 72 hours after collections. The differences of LFs contents between unfiltered and filtered AP-PCs in 4 hours, 24 hours, 48 hours, 72 hours, 96 hours after collections were 14. 5, 23. 2, 17. 6, 11.3 and 2. 5 WBCs/μl, respectively.There was statistically significant difference between unfiltered and filtered samples (Fbetween subjects=9. 216,P < 0. 05). The differences were considerable within 48 hours, and then declined gradually. The results of bivariate correlation analysis showed that there were no statistically significant correlation between PLT concentrations and LFs contents (at 4, 24, 48, 72, 96 hours after collections the correlation coefficients rs were -0.002, 0.015, 0.027, 0.042 and 0. 037,respectively,P2-tailed>0.05). ConclusionsRQ-PCR and FCM can be used to quantitate LFs in AP-PCs. The concentration of LFs in AP-PCs is influenced by storage time and filtration, but it is not affected by PLT concentration.
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<p><b>OBJECTIVE</b>To investigate gene expression profile in nasopharyngeaL carcinoma (NPC) cell lines with different metastatic potentialities, in order to identify new candidate genes related to the development, progress and metastasis of NPC.</p><p><b>METHODS</b>The mRNA expressions of high metastatic NPC cell line 5-8F, tumorigenic but nonmetastatic NPC cell line 6-10B and non-tumorigenic NPC cell line 13-9B (3 sublines of SUNE-1) were investigated by cDNA microarray containing 14 000 cDNA clones. The alterations in gene expression levels were confirmed by reverse-transcription PCR.</p><p><b>RESULTS</b>There were 82 differentially expressed genes comparing 5-8F and 13-9B; 38 differentially expressed genes comparing 6-10B and 13-9B; 54 comparing 5-8F and 6-10B. There were 12 common differentially expressed genes comparing 6-10B, 5-8F and 13-9B; 14 common differentially expressed genes comparing 5-8F and 13-9B, 6-10B. The expressions of the above genes were involved in metabolism, transcription, differentiation, apoptosis and signal transduction.</p><p><b>CONCLUSION</b>The gene expression profile in nasopharyngeal carcinoma cell lines is an important index in the search of new candidate genes related to NPC.</p>
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Humans , Cell Line , DNA, Complementary , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Nasopharyngeal Neoplasms , Genetics , Pathology , Neoplasm Metastasis , Genetics , Oligonucleotide Array Sequence Analysis , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To effectively screen p16 protein expression of different clinical stage nasopharyngeal carcinoma (NPC) by constructing and applying high-throughput tissue microarray/tissue chip.</p><p><b>METHODS</b>A series of tissue chips were prepared by using tissue arrayer with samples from different clinical stage NPC tumors and noncancerous nasopharynx tissue. Specimens from 259 cases of nasopharyngeal lesions were detected immunohistochemically on a tissue chip for p16 protein expression and the correlation of p16 protein expression to clinical stage of NPC was analyzed statistically.</p><p><b>RESULTS</b>p16 protein expression was detected in all 18 histologically normal nasopharyngeal epithelia. No p16 protein was detected in 3 of 3 (100%) stage I NPC, 38 of 44 (86.3%) stage II NPC, 59 of 68 (86.8%) stage III NPC, 23 of 28 (82.1%) stage IV NPC, 87 of 98 (88.8%) unclear stage NPC. The efficiency of p16 protein expression in NPC tissues was significantly lower than that in normal nasopharyngeal epithelia (chi(2) = 82.58, P < 0.001), and there was no apparent relationship between p16 protein expression and clinical stages (chi(2) = 0.09, P = 0.769).</p><p><b>CONCLUSIONS</b>The frequent deletion of p16 protein in NPC suggests that p16 gene has an important role in the development and progression of NPC. The consistency of p16 protein deletion in different stages of NPC suggests that the deletion of p16 protein is an early event in the development of NPC, and it is feasible to utilize tissue microarray for a rapid, economic and accurate screening of clinical tissue specimens on a large scale.</p>
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Humans , Cyclin-Dependent Kinase Inhibitor p16 , Immunohistochemistry , Nasopharyngeal Neoplasms , Metabolism , Pathology , Neoplasm StagingABSTRACT
Objective To obtain genes encoding the novel molecules for diagnosis of schistosomiasis.Methods Juvenile S.japonicum cDNA library was immunoscreened to obtain positive clones.By DNA sequencing and sequence analysis,the target gene was amplified by PCR and subcloned into prokaryotic plasmid pET28a.The recombinant plasmid was transformed into E.coli BL21 followed by expression of the protein induced by IPTG.The protein was identified by Western blotting.Results 34 positive clones were obtained,24 of which were chosen to be sequenced,13 of which were Sj22600 gene.The protein were recognized with sera of infected rabbits and patients with acute and chronic schistosomiasis by Western blotting.Conclusion The gene coding for Sj22600 membrane protein was screened with high frequency in the cDNA library.The E.coli BL21 transformed with the recombinant plasmid can express the fusion protein,which shows immunoactivity.
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The in vitro tumoricidal activity of peritoneal macrophages harvested from C57BL mice and activiated by li posomes containing water-soluble muramyl dipeptides (MDP) was measured by ~(125)I.UdR release assay. The results demonstrated that liposomes containing MDP could effectively activiate macrophages to become tumoricidal. The percentage of pu(?)monarymetastasis and the average metastatic pulmonary colonies of mice with experimental tumor metastasis decreased after intravenous injection of MDP encapsulated in liposomes. These results suggested that systemic administration liposomes containing MDP whichinduced macrophage activiation might provide a useful immunot heray for tumor, especial1y for pulmonary mini metastasis.