This decrease indicated the production of 1O2, which can irrevers

This decrease indicated the production of 1O2, which can irreversibly react with DMA. Moreover, the generation curve of ZnPc4-loaded Aurod@pNIPAAm-PEGMA nanogels was similar with that of pure ZnPc4, demonstrating that the capacity of generating 1O2 of ZnPc4 was hardly affected after being loaded in Aurod@pNIPAAm-PEGMA nanogels. It is thus suggested that the Aurod@pNIPAAm-PEGMA nanogel might be a promising drug carrier for photodynamic therapy

in the future. Figure 9 The generation profiles of singlet oxygen from ZnPc 4 -loaded Au rod @pNIPAAm-PEGMA nanogels (Au/P). The nanogels were irradiated by an 808-nm laser and a 680-nm LED lamp, respectively. In vitro PDT study on Hela cells The in vitro PDT study, represented in Figure 10,

showed the percentage of cell viability after treatment of Hela cells with the ZnPc4-loaded Aurod@pNIPAAm-PEGMA nanogel (300 μg/mL) at different irradiated conditions. Compared with the cells’ group Navitoclax order with no light treatment, no significant difference of the cell viability was found in the 808-nm laser-treated group. However, for the 680-nm light-treated group, the cell viability decreased www.selleckchem.com/products/4-hydroxytamoxifen-4-ht-afimoxifene.html to 40%. It is interesting to note that when irradiated by the two lights, the cell viability decreased to 10%. This is because the 808-nm laser treatment might result in the release of ZnPc4 from nanogels, which could improve the efficiency of the generation of singlet oxygen after the 680-nm irradiation and thus enhance the PDT effect on Hela cells. Figure 10 The photodynamic therapy effect of ZnPc 4 -loaded Au rod @pNIPAAm-PEGMA nanogels on Hela cells at different irradiated conditions. Conclusions A facile approach to check details prepare near-infrared-responsive Cobimetinib Aurod@pNIPAAm-PEGMA nanogels was described. The LCSTs of these Aurod@pNIPAAm-PEGMA nanogels could be tuned by changing the molar ratio of NIPAAm/PEGMA. The release of ZnPc4 loaded in Aurod@pNIPAAm-PEGMA nanogels increased with the extension of irradiated time and the increase of the power

of the NIR laser. The loaded ZnPc4 in Aurod@pNIPAAm-PEGMA nanogels could generate singlet oxygen efficiently. The in vitro study showed obvious PDT effect on Hela cells. On these bases, the Aurod@pNIPAAm-PEGMA nanogels might serve as a promising drug carrier in PDT. Authors’ information RL, TXH, and LDH are Ph.Ds. and professors. ST, WCD, KXB, YAQ, and CM are M.D. students in the Department of Biomaterials, College of Materials, Xiamen University. Acknowledgments This work was financially supported by the National Basic Research Program of China (2010CB732402, 2013CB933703) and the National Natural Science Foundation of China (30970733, 81171448). References 1. Han G, Ghosh P, Rotello VM: Functionalized gold nanoparticles for drug delivery. Nanomedicine 2007, 2:113–123.CrossRef 2. Lal S, Clare SE, Halas NJ: Nanoshell-enabled photothermal cancer therapy: impending clinical impact.

Environmental stimuli are sensed through transient [Ca2+]i elevat

Environmental stimuli are sensed through transient [Ca2+]i elevations by M. loti To further validate the experimental system, abiotic stimuli which are known to trigger [Ca2+]i changes in both plants [23] and cyanobacteria [18, 19] were applied to apoaequorin-expressing M. loti cells. A mechanical perturbation, simulated by the injection of isoosmotic cell culture medium, resulted in a rapid Ca2+ transient increase (1.08 ± 0.24 μM) that decayed within 30 sec (Fig. 1A). This Ca2+ trace, which is frequently referred to as a “”touch response”", is often observed after the

hand-operated injection of any stimulus [24]. A similar Ca2+ response characterized by an enhanced Ca2+ peak of 2.14 ± 0.46 μM was triggered by a find more simple injection of air into the cell suspension with a needle (Fig. 1A). Figure 1 Ca 2+ measurements in M. loti

cells stimulated with different physico-chemical signals. Bacteria were challenged (arrow) with: A, mechanical perturbation, represented by injection of an equal volume of culture medium (black trace) or 10 volumes of air (grey trace); B, cold shock, given by 3 volumes of ice-cold culture medium (black SBE-��-CD chemical structure trace); control cells were stimulated with 3 volumes of growth medium kept at room temperature (grey trace); C, hypoosmotic stress, given by injection of 3 volumes of distilled water (black trace); salinity stress, represented by 200 mM NaCl (grey trace); D, different external Ca2+ concentrations. These and the following traces have been chosen medroxyprogesterone to best represent the average results of at least three independent experiments. Cold and hypoosmotic shocks, caused by supplying three volumes of ice-cold medium and distilled water, respectively, induced Ca2+ traces with distinct kinetics, e.g. different Selleck Autophagy Compound Library height of the Ca2+ peak (1.36 ± 0.13 μM and 4.41 ± 0.51 μM, respectively) and rate

of dissipation of the Ca2+ signal (Fig. 1B and 1C). As a control, cells were stimulated with three volumes of growth medium at room temperature, (Fig. 1B) resulting in a Ca2+ trace superimposable on that of the touch response (Fig. 1A). These findings eliminate the possible effect of bacterial dilution on changes in Ca2+ homeostasis. Challenge of M. loti with a salinity stress, which has recently been shown to affect symbiosis-related events in Rhizobium tropici [25], resulted in a [Ca2+]i elevation of large amplitude (3.36 ± 0.24 μM) and a specific signature (Fig. 1C). Variations in the extracellular Ca2+ concentration determined the induction of transient Ca2+ elevations whose magnitude was dependent on the level of external Ca2+. After a rapidly induced increase in [Ca2+]i, the basal Ca2+ level was gradually restored with all the applied external Ca2+ concentrations (Fig. 1D), confirming a tight internal homeostatic Ca2+ control, as previously shown for other bacteria [14, 18]. All the above results indicate that aequorin-expressing M.

In agreement with data presented here,

In agreement with data presented here, Takamatsu et al. showed that CC1 isolates contained all srt genes, whereas CC29 isolates lacked srtBCD genes [34]. However, none of our serotype 9 isolates contained the srtBCD gene cluster, whereas this cluster was detected in a Japanese serotype 9 isolate [34]. This could imply geographical variation. Moreover, the

revs gene is absent from all cluster B isolates, with the exception of cluster B5 isolates. This regulator influences expression of putative virulence factors [35]. Therefore, lack of revs might affect virulence of isolates. The IgA1 protease gene was found to be absent in all serotype 9 isolates, and displayed extensive sequence variation in serotype 7 isolates. All serotype 2 isolates including the avirulent isolates contained the IgA1 protease gene. Zhang et al. showed that most selleck chemical pathogenic serotype 2 isolates contained CB-839 manufacturer the IgA1 protease gene, whereas the gene was sparsely found in non-invasive serotype 2 isolates [36]. In the latter study mainly isolates obtained in China were used. Sequence variation among isolates belonging to cluster B was observed for other putative virulence genes as well, like ofs, glnA, fbps and apuA. The ofs gene was highly conserved among virulent serotype

1 and 2 isolates but showed extensive sequence diversity in avirulent serotype 2 and serotype 7 isolates, as was also described by Takamatsu et al [15]. Interestingly, at least two of the ofs positive serotype 7 strains do not express OFS in vitro, as shown in the serum opacification assay [37]. This suggests the presence of silent ofs genes. A silent epf gene was present in isolates in cluster B3. Two of the B3 isolates (22083R1 and 8186) expressed the enlarged version of MRP, but none of the probes used for the CGH hybridized to the mrp gene, suggesting extensive DNA ligase sequence variation exists between different serotype 9 isolates. The presence of a mrp gene in the two isolates was Idasanutlin cell line confirmed

by PCR analysis (data not shown). Serotype 9 isolates were distributed among 2 virulence clusters, V6 and V7 that differed considerably in their distribution of putative virulence genes. This suggests differences in virulence exist among serotype 9 isolates that were not identified in our experimental infection model. Avirulent MRP-EF- serotype 2 isolates clustered together with serotype 7 isolates both by CGH as well as by MLST. Such a clustering is in agreement with previous studies [24, 25]. The clustering strongly suggests similarity in genetic background between the isolates and could suggest that the avirulent serotype 2 isolates originated from serotype 7 isolates after the exchange of the capsular genes. Capsular exchange has been described for other streptococci like GBS [38] and Streptococcus pneumonia [39].

References 1 Legler JM, Ries LA, Smith MA, et al : Cancer survei

References 1. Legler JM, Ries LA, Smith MA, et al.: Cancer surveillance series [corrected]: brain and other central nervous system cancers: recent trends in incidence and mortality. J Natl Cancer Inst 1999, 91 (16) : 1382–90.CrossRefPubMed 2. Addeo R, Casale

F, Caraglia M, et al.: Glucocorticoids induce G1 arrest of PR-171 price lymphoblastic cells through retinoblastoma protein Rb1 dephosphorylation in childhood acute lymphoblastic leukemia in vivo. Cancer Biol Ther 2004, 3 (5) : 470–6.PubMed 3. Casale F, D’Angelo V, Addeo R, Caraglia M, et al.: P-glycoprotein 170 expression and function as an adverse independent prognostic factor in childhood acute lymphoblastic leukemia. Oncol Rep 2004, 12 (6) : 1201–7.PubMed 4. Steelman LS, Abrams SL, Whelan J, et al.: Contributions of the Raf/MEK/ERK, PI3K/PTEN/Akt/mTOR and Jak/STAT pathways to leukemia. Leukemia 2008, 22 (4) : 686–707.CrossRefPubMed www.selleckchem.com/JNK.html 5. Kuntzen C, Sonuc N, De Toni E, et al.: Inhibition of c-Jun-N-terminal-kinase sensitizes tumor cells to CD95-induced apoptosis and induces G2/M cell cycle arrest. Cancer Res 2005, 65 (15) : 6780–8.CrossRefPubMed 6. Gregorj C, Ricciardi MR, Petrucci MT, et al.: ERK1/2 phosphorylation is an independent predictor of complete remission in newly diagnosed adult acute lymphoblastic leukemia. Blood 2007, 109 (12) this website : 5473–6.CrossRefPubMed 7. Milella M, Kornblau SM, Estrov Z, et al.: Therapeutic targeting of the MEK/MAPK

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Gadd45 gene family which functions in negative growth control. Oncogene 1999, 18: 4899–4907.CrossRefPubMed 9. Gupta M, Gupta SK, Balliet AG, et al.: Hematopoietic cells from Gadd45a- and Gadd45b-deficient mice are sensitized to genotoxic-stress-induced apoptosis. Oncogene 2005, 24: 7170–7179.CrossRefPubMed 10. Harada K, Toyooka S, Shivapurkar N, et al.: Deregulation of caspase 8 and 10 expression in pediatric tumors and cell lines. Cancer Res 2002, 62 (20) : 5897–901.PubMed 11. Kornblau SM, Womble M, Qiu YH, et al.: Simultaneous activation of multiple signal transduction check details pathways confers poor prognosis in acute myelogenous leukemia. Blood 2006, 108 (7) : 2358–65.CrossRefPubMed 12. Kharas MG, Fruman DA: ABL oncogenes and phosphoinositide 3-kinase: mechanism of activation and downstream effectors. Cancer Res 2005, 65 (6) : 2047–53.CrossRefPubMed 13. Masera G, Conter V, Rizzari, et al.: AIEOP Non-B ALL trials. Int J Pediatric Hematol Oncol 1999, 6: 101. 14. Bennet JM, Catovsky D, Daniel MT, et al.: The morphological classification of acute lymphoblastic leukemia: concordance among observers and clinical correlation. Br J Haematol 1981, 9 (6) : 1012. 15. Barry OP, Mullan B, Sheehan D, et al.: Constitutive ERK1/2 activation in esophagogastric rib bone marrow micrometastatic cells is MEK-independent. J Biol Chem 2001, 276: 15537–15546.

Lipid microspheres (LM) were target-drug delivery carriers which

Lipid microspheres (LM) were target-drug delivery carriers which could congregate selectively in the site such as inflammation or injuring blood vessel and change the distribution of drugs in vivo [13, 14]. Flurbiprofen axetil injection, 0.2 μm in diameter, was composed of lipid microspheres

and flurbiprofen axetil[15]. It was target-congregated easily to tumor, especially malignant tumor for there had abundant Caspase inhibitor fresh capillary vessel and released inflammatory factor. The latter could enlarge the fissure of endothelium cells and let it be taken up by macrophages and neutrophils. So, the biosynthesis of prostaglandin was restrained, and the analgesic effects of flurbiprofen axetil would be appeared [16]. Flurbiprofen axetil injection this website always had better analgesic effects in bone metastasis of tumor while nociceptor pain was mainly expressed [9]. Anaesthetic anodynes were always used in moderate and severe pain patients. It acted in central nerve system, and the analgesic effects was not relative with the site or kind of pain. But, side effects always happened,

such as constipation, breath inhibition, drug dependence, even exciting central nerve system when it was used for long time [2]. Flurbiprofen axetil and other NSAIDs drugs acted in the site of distal nerve. Its analgesic effects were always not bad than anaesthetic anodynes when the inflammatory medium was liberated in the site of muscle, tendon, ligament, and bone. It could be used as first line anodyne and combined with anaesthetic anodynes in corresponding cancer pain [4]. Our results showed that PD0332991 mw intravenous flurbiprofen axetil had better analgesic effect to cancer pain with bone or vertebra metastasis. It could reduce the dosage of the anaesthetic drugs, or increase CYTH4 the analgesic effects with little side effect, especially in patient who had constipation or had a tendency of ileus. Our results showed the analgesic effect was better than the Ou Yang’s report [9], and

similar to the report by Xu et al [17]. Perhaps for the reason of insufficient cases, we found that flurbiprofen axetil had slight analgesic effect to cancer pain in abdomen. The half-life time of flurbiprofen axetil was 5.8 hours. Its onset of action was about 15 minutes after being used, and continued about 3 hours in post-operation. When it was used in cancer patients, it began to work quickly about in 30 minutes, and the duration of action was about 9 hours [18]. So it was especially suitable for breakthrough pain to the patient who were using anaesthetic anodyne. We found that most patients could obtain analgesic effects after being added flurbiprofen axetil 50 mg while their pain could not be controlled by anaesthetic drugs. But in some patients, the analgesic effect was only maintained 3–4 hours.

Evol Appl 3:538–546CrossRef Gundel PE, Zabalgogeazcoa I, Vázquez

Evol Appl 3:538–546CrossRef Gundel PE, Zabalgogeazcoa I, Vázquez de Aldana BR (2011)

Interaction between plant genotype and the symbiosis with Epichloë fungal endophytes in seeds of red fescue (Festuca rubra). Crop For Sci 62:1010–1016 Gundel PE, Garibaldi LA, Martínez-Ghersa MA, Ghersa CM (2012) Trade-off between seed number and weight: influence of a grass-endophyte symbiosis. Basic Appl Ecol 13:32–39CrossRef Hahn HM, McManus T, Warnstorff K, Monahan BJ, Young CA, Davies E, Tapper BA, Scott B (2008) Neotyphodium fungal endophytes confer physiological protection to perennial ryegrass (Lolium perenne L.) subjected to a water deficit. Environ Exp Bot 63:183–199CrossRef Hamilton CE, Bauerle, TL (2012) A new currency for mutualism: Neotyphodium antioxidants and host drought response. Fungal Divers Hamilton CE, Faeth SH, Dowling TE (2009) Distribution MLN2238 of hybrid fungal symbionts and environmental stress. Microbial Ecol 58:408–413CrossRef Hamilton CE, Dowling TE, Faeth SH (2010) Hybridization in endophyte symbionts alters host response to moisture and nutrient treatments. Microb Ecol 59:768–75PubMedCrossRef Harman GE (2000) Myths and dogmas of biocontrol: changes in perceptions derived from research on Trichoderma harzianum T-22. Plant Dis 84:377–GS-4997 price 393CrossRef

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Table 3 Quantity of alcohol in the standard size for each alcohol

Table 3 Quantity of alcohol in the standard size for each alcohol Alcohol Size ml % Ethanol (g) Beer 1 medium

bottle 500 5 20 Sake (Japanese rice wine) 1 go (Japanese unit) 180 15 22 Whisky or SB431542 manufacturer Brandy double 60 43 20 Shochu (Japanese liquor 35°) 1 go (Japanese unit) 180 35 50 Wine 1 glass 129 12 12 CKD clinical guidelines 2009 Table 4 Quantity of alcohol in a standard drink of each country Country Ethanol (g) Range (g) USA 12 9.3–13.2 Canada 13.6 13.6 UK 9.5 8–10 Europe 9.8 8.7–10.0 AUS and NZ 9.2 6.0–11.0 Japan 23.5 21.2–28.0 O’Shea RS, et al. Alcoholic liver disease. Hepatology. 2010;51(1):307–28 Bibliography 1. White SL, et al. Nephrol Dial Transplant. 2009;24:2464–72. (Level 4)  

2. Yamagata K, et al. Kidney Int. 2007;71:159–66. (Level 4)   3. Funakoshi Y, et al. learn more Environ Health Prev Med. 2012;17:199–204. (Level 4)   4. Menon V, et al. Nephrol Dial Transplant. 2010;25:3301–7. (Level 4)   5. Shankar Go6983 manufacturer A, et al. Am J Epidemiol. 2006;164:263–71. (Level 4)   6. Knight EL, et al. Nephrol Dial Transplant. 2003;18:1549–54. (Level 4)   7. Reynolds K, et al. Kidney Int. 2008;73:870–6. (Level 4)   8. Schaeffner ES, et al. Arch Intern Med. 2005;165:1048–53. (Level 4)   Does exercise affect the onset or progress of CKD? Inactivity and lower health-related quality of life (HRQOL) are regarded as risk factors for mortality and hospitalization in patients with dialysis. However, little has been reported about the effect of exercise on the onset or progress of CKD. Heiwe et al. reported in a systematic review (45 studies with 1863 adult participants with CKD) that there was evidence for significant beneficial effects of regular exercise on physical fitness, walking capacity, of cardiovascular dimensions (e.g. blood pressure

and heart rate), HRQOL and some nutritional parameters. However, the result of the relationship between exercise and urinary protein or GFR was controversial. For obese patients with CKD, exercise improved body weight, blood pressure and urinary protein. The risk of cardiac events (arrhythmia, ischemic heart disease, and sudden death) during exercise is well known in patients with CKD. Therefore, when patients are prescribed exercise, it is essential to assess every patient’s activity, exercise tolerance, and risk of cardiovascular disease. Bibliography 1. Heiwe S, et al. Cochrane Database Syst Rev. 2011;10:CD003236. (Level 1)   2. Leehey DJ, et al. Cardiovasc Diabetol. 2009;8:62. (Level 2)   3. Pechter U, et al. Int J Rehabil Res. 2003;26:153–6. (Level 4)   4. Kosmadakis GC, et al. Nephrol Dial Transplant. 2012;27(3):997–1004. (Level 3)   5. Eidemak I, et al. Nephron. 1997;75:36–40. (Level 2)   6. Boyce ML, et al. Am J Kidney Dis. 1997;30:180–92. (Level 4)   7. Afshinnia F, et al. Nephrol Dial Transplant. 2010;25:1173–83.

Isokinetic and isotonic measurements of knee extension and flexio

Isokinetic and isotonic measurements of knee extension and flexion, in that they involve translating a weight along an arc of motion within a given time interval, are measures of muscle power (although they are mostly reported as joint torques

in feet pounds or Newton meters) whereas isometric measurements involve purely the ability to generate force. Because these loading conditions are more relevant to human motion, most studies have reported results of isokinetic and isotonic exercise. Table 1 summarizes results of cross-sectional learn more studies of lower-extremity muscle function [68–73]. In cross-sectional studies comparing young normal subjects in the 20–40-year age range to healthy elders in the 70–80-year age range, declines in knee

extensor torque and power have ranged from 20% to 40%, with greater losses in the 50% range reported for individuals in their 1990s [74–78]. Over the lifetime, men have inherently greater knee extensor power and torque than women, but on a percentage basis, age-related losses are similar between genders, with losses in men incurring greater MK-4827 research buy absolute losses because they start with CB-5083 higher baseline values. Compared to the abundance of cross-sectional studies, there are fewer longitudinal studies of knee extensor properties with aging. Hughes et al. examined a cohort of 52 elderly men and 68 women who had been examined 10 years earlier, finding similar declines in the knee extensors and flexors ranging from 12% to 18% per decade [79]. Longitudinal studies of smaller cohorts have shown variable results, with one study reporting losses of roughly 3% per year in 23 men aged 73–86 at baseline [80], and another study which reported no changes in strength of either men or women over an 8-year follow-up

[81]. Cross-sectional studies Thalidomide of isometric measurements of ankle plantar flexion have shown age-related declines similar to those measured for knee extension torque and power. Studies of age-related muscle strength in the upper extremities show essentially similar results to the lower extremities, with cross-sectional studies reporting declines of 20–40% in measures such as hand-grip strength and elbow extension torque between healthy younger subjects and elderly subjects and longitudinal studies showing yearly declines ranging from 1% to 5% [17]. Table 1 Age-related changes in muscle power and muscle strength Study Gender Measurement/joint/movement Age range (years) Study design Changes with aginga Dean et al. 2004 [73] F IK/hip/FLX, EXT 21–82 CS ↓22–33% Johnson et al. 2004 [72] F IK, IM/hip/AD, AB 21–91 CS ↓24–34% IK, ↓44–56% IM Kubo et al. 2007 [71] M IM/ankle/PF 20–77 CS ↓40% Morse et al. 2005 [70] M IM/ankle/PF 25.3 ± 3.5–73.8 ± 3.5 CS ↓47% Petrella et al.

c-FLIP is generally expressed in embryonic tissues, but is not ex

c-FLIP is generally expressed in embryonic tissues, but is not expressed in most normal adult tissues, whereas is over-expressed in

the majority of human cancers. It indicates that c-FLIP may associate with the tumorigenesis and progress of most human cancers. Published information regarding the significance of c-FLIP over-expression Selonsertib order in human tumors has only recently begun to accumulate [21–24]. Human HCCs show resistance to apoptosis mediated by several death receptors. c-FLIP is constitutively expressed in human HCC cell lines, and is expressed with a higher positive rate in human HCC tissues than in noncancerous liver tissues. In the present study, positive immunostaining was detected for c-FLIP in 83.72% of human HCC samples, but was absent from normal hepatic tissues. The other authors’ and our studies suggest that c-FLIP may play an important role in human HCCs. For the patients with c-FLIP overexpression, they may have a shorter recurrence-free survival time. Now, RNAi, that can induce Staurosporine highly specific target gene silencing in mammalian cells using siRNA, has find protocol been a powerful tool in studying the cell function of any gene. c-FLIP expression can be inhibited by RNA interference using siRNAs, evidence from reduced levels

of c-FLIP mRNA and c-FLIP protein[25]. In this study, the c-FLIP-targeted siRNA vectors were designed to specifically silence next c-FLIP. Then, the plasmids transcript

containing c-FLIP-targeted siRNA and negative siRNA were constructed and transfected into 7721 cells. We found that there were significant differences between 7721/pSuper-Si1 and 7721/pSuper-Neg in c-FLIP expression at both mRNA and protein levels (Figure. 3A, Figure. 3B). The phenomenon that screened positive clone with lower c-FLIP expression indicated that the c-FLIP-targeted siRNA inhibited c-FLIP expression specifically. Some studies reported that siRNA-mediated silencing of c-FLIP induced spontaneous apoptosis in a panel of p53 wild-type, mutant, and null colorectal cancer cell lines [11]. And the anti-apoptotic role of c-FLIP in regulating TRAIL-mediated apoptosis in colon cancer cells was clearly shown using siRNA methodology [26]. Furthermore, c-FLIP down-regulation sensitized colorectal cancer cells to chemotherapy [27]. And, specific silencing of c-FLIPL was sufficient to sensitize MDA435 cells to doxorubicin. Our study showed that c-FLIP gene silencing enhanced doxorubicin-induced HCC cell apoptosis (Figure. 5). These results indicate that c-FLIP may be an important regulator of chemotherapy-induced cell death in human HCC cells. Conclusion The results of the present investigation demonstrated that c-FLIP is frequently expressed in human HCCs, correlated with Edmondson standard. The HCC patients with c-FLIP overexpression may have a shorter recurrence-free survival time.

J Cell Sci 2003, 116 (Pt 17) : 3543–3556 CrossRefPubMed 31 van ‘

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and endothelial human CLCA2 mediate lung metastasis. J Biol Chem 2001, 276 (27) : 25438–25446.CrossRefPubMed 39. Price JT, Tiganis T, Agarwal A, Djakiew D, Thompson EW: Epidermal growth factor promotes MDA-MB-231 breast cancer cell migration through a phosphatidylinositol 3′-kinase and phospholipase C-dependent mechanism. Cancer Res 1999, 59 (21) : 5475–5478.PubMed Montelukast Sodium 40. Yang Z, Bagheri-Yarmand R, Wang RA, Adam L, Papadimitrakopoulou VV, Clayman GL, El-Naggar A, Lotan R, Barnes CJ, Hong WK, Kumar R: The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses c-Src and Pak1 pathways and invasiveness of human cancer cells. Clin Cancer Res 2004, 10 (2) : 658–667.CrossRefPubMed 41. Giannelli G, Antonaci S: Biological and clinical relevance of Laminin-5 in cancer. Clin Exp Metastasis 2000, 18 (6) : 439–443.CrossRefPubMed Competing interests PJM is Vice-President of Biology Applications at Amnis Corporation and owns stock in Amnis Corporation.