YHS and XPH performed the experiments and were involed in drafting the article. All authors have read and approved the final manuscript.”
“Introduction Lung cancer is one of the leading causes of cancer-related mortality both in China and throughout the world [1, 2]. Non-small cell lung cancer (NSCLC) accounts for75-80% of all lung cancer [3]. Standard therapeutic strategies such as surgery, chemotherapy, or radiotherapy have

reached a plateau [1]. Significant advances in the research of the biology and molecular mechanisms of cancer have allowed the development of new molecularly targeted agents for the treatment of NSCLC [4–8]. One such target is the epidermal growth factor receptor Selumetinib mw (EGFR), a 170-kDa trans-membrane glycoprotein and member of erbB family. Small molecule tyrosine kinase inhibitors (TKI), such as gefitinib and erlotinib, disrupt EGFR kinase activity by binding the adenosine triphosphate pocket within the catalytic region of the tyrosine kinase domain [9]. Currently, both

gefitinib and erlotinib are used for treatment of patients with advanced NSCLC. TKI clinical trials have shown that these agents have dramatic effect on the subset of NSCLC patients with somatic mutations in the tyrosine kinase domain of the EGFR gene, whereas the presence of KRAS mutations seems to be correlated with primary resistance to these agents [10–15]. So it is necessary to identify the mutation status of KRAS and EGFR for selection Cilomilast of patients who are more likely to benefit from TKI. Although almost 70% of patients with NSCLC present with locally advanced or metastatic disease at the

time of diagnosis [16, 17], KRAS and EGFR mutation status is most commonly assessed only in the primary tumor tissue based on the assumption that primary and metastases are pathologically concordant. from However, it has been known that lung cancers are often heterogeneous at the molecular level even within the same tumor and many key molecular alterations may occur during metastatic progression [18–20]. It is still unclear whether KRAS and EGFR mutation status in primary tumors is reflected in their corresponding metastases in Chinese patients with NSCLC, although several recent relevant studies in western countries have been performed and published [21–26]. In the present study, we investigate KRAS and EGFR mutation status using PCR-based sequencing analyses in 80 primary tumor samples and their corresponding local lymph node metastases from Chinese patients with NSCLC. The goal is to determine whether KRAS and EGFR mutation profile is stable during the metastatic progress and to investigate the clinical usefulness of mutational analyses in primary tumor versus in metastases for planning EGFR-targeted therapies for the treatment of patients with NSCLC.

2008). It might also be of use in Stark spectroscopy experiments on isolated and non-randomly aligned complexes, e.g., in oriented lamellar aggregates. (Stark spectroscopy deals with the effects of applied electric fields on the absorption or emission spectrum of a molecule (Boxer 1996).)

The dependency of the so-called electrochromic absorbance changes on the orientation of the molecules arises from the fact that the field-induced frequency shift of a given absorbance band depends on the relative orientation of the field vector and selleck screening library the transition dipole moment vector of the molecule; in molecules possessing permanent dipole moments, it also depends on the difference between the ground- and excited-state polarizability of the field-indicating pigment molecules (Junge 1977). The orientations of the transition dipole moments are functionally very important: they strongly influence the rates and the routes of excitation energy transfer in the pigment system, which depends on the mutual orientation of the transition dipoles of the acceptor and donor molecules (Van Grondelle et al. 1994). With regard to the excitation energy distribution, excitonically coupled molecules, which usually give rise to characteristic CD bands (see below), and influence the absorbance and

fluorescence properties, are of special interest. Since these also depend on the mutual orientation of the corresponding transition dipoles of the interacting molecules, LD data are also of paramount importance in this respect. Circular dichroism Circular dichroism (CD) refers to the phenomenon where the left- and right-handed circularly polarized light are absorbed to a different extent. CD is VX-809 price usually defined as the (wavelength-dependent)

difference in absorption of the left- and the right-handed circularly polarized light: CD = A L − A R. CD arises from the intra- or intermolecular asymmetry (helicity) of the molecular structure. The helicity (chirality or handedness) of the structure means that it cannot be superimposed on its mirror image. As the handedness of a structure is the same from any direction, CD can be observed in randomly oriented samples. (In fact, the general theories are given for spatially averaged samples.) CD signals can originate from different molecular systems of different complexity, and they can give rise to different bands of different physical origins: AZD9291 manufacturer (i) In the basic case, CD arises from intrinsic asymmetry or the asymmetric perturbation of a molecule (Van Holde et al. 1998). For a single electronic transition, CD has the same band shape as the absorption, and its sign is determined by the handedness of the molecule (often referred to as positive or negative Cotton effect). (ii) In molecular complexes or small aggregates, CD is generally induced by short-range, excitonic coupling between chromophores (Tinoco 1962; DeVoe 1965). Excitonic interactions give rise to a conservative band structure (i.e.

“
“Background Group III-V semiconductors containing small amounts of bismuth (Bi), popularly known as ‘dilute bismide,’ attracted selleckchem great attention in the past decade. Bismuth

is the largest and the heaviest group V element with its isoelectronic energy level that resides in the valence band of most III-V materials. Incorporation of a small amount of Bi atoms in a common III-V compound is expected to lead to a large bandgap reduction [1] and strong spin-orbit splitting [2]. This provides a new degree of freedom to engineering the band structure for potential optoelectronic and electronic device applications. Under such conditions, it is expected that troublesome hot-hole-induced Auger recombination and inter-valence band absorption (IVBA) processes can be suppressed leading to high efficiency and temperature insensitive lasers for optical communications [3]. Most published literatures so far focus on growth and material properties of GaAsBi with improving quality, making GaAsBi closer to device applications. GaAsBi light-emitting diodes (LEDs) [4] and optically pumped [5] and electrically injected [6] laser diodes have been demonstrated recently. Group III-V semiconductor phosphides are important

materials for optoelectronic devices working at visible and near-infrared wavelength range [7, 8]. The incorporation of Bi into InP can further extend transition wavelengths for optoelectronic devices with aforementioned improved device performances as a result of the suppressed PRKD3 Auger recombination and IVBA processes. Berding et al. theoretically compared InPBi, InAsBi, InSbBi, and HgCdTe, and pointed out that InPBi was much more robust MLN8237 than the others, thus making it as a promising candidate for infrared applications. However, their calculations also showed that InPBi was very difficult to synthesize due to a larger miscibility gap than that of InAsBi and InSbBi [9]. So far, a few works on the optical studies of InP/Bi where the incorporated Bi is only in the doping level [10, 11] were reported. The spectroscopy reveals rich sharp transitions at energy levels close to the InP bandgap at low temperatures. In this work, we investigate the structural and optical properties

of InPBi with Bi composition in the range of 0.6% to 2.4%. The Bi-induced bandgap reduction of around 56 meV/Bi% is obtained. Strong and broad photoluminescence (PL) signals have been observed at transition energy much smaller than the InPBi bandgap. Methods The samples were grown on (100) semi-insulating InP substrates by V90 gas source molecular beam epitaxy (GSMBE). Elemental In and Bi and P2 cracked from phosphine were applied. After the surface oxide desorption of InP substrate at 524°C, a 75-nm undoped InP buffer was grown at 474°C, the normal growth temperature of InP. Then the growth temperature was decreased significantly for InPBi growth. Both the Bi/P ratio and the growth temperature were adjusted to achieve InPBi with various Bi compositions.

Bentzen et al. reported enhanced RT-induced pulmonary fibrosis in patients treated with concomitant tamoxifen [29]. This effect was not observed in our cohort of patients. In accordance with Wennemberg et al. [25] no correlation was found between HU and either chemotherapy or TAM. Nevertherless the very low incidence

Talazoparib order of lung toxicity was certainly also related, in our series, to the very low values of doses administered to the lung volume as shown from the calculated dose volume histograms. Statistically significant changes in toxicity ≥G2 and ≥G1 based on DLCO (p = 0.006 and p = 0.034, respectively) were detected when comparing data of patients who did receive chemo-therapy and those who did not, but no adjunctive effects were seen due to radiotherapy. These findings are in accordance with the low observed mean DLCO caused by the adjuvant chemotherapy [27, 30]. This confirms that DLCO is a more sensitive variable of functional pulmonary changes due to drug-induced toxicity. These differences were lost at Selleck GSI-IX 2 years post-radiotherapy indicating recovery over time and no additional influence of hypo-fractionated radiotherapy schedule. These results confirm the literature [27], indicating a trend towards normalization at 5 months after radiotherapy. FEV1% showed a significant correlation

with smoking habits for ≥G1 toxicity at 2-years post-radiotherapy. Our findings support the hypothesis that this new hypofractionated schedule neither implies a detriment of functional breathing nor hinders Mannose-binding protein-associated serine protease the recovery over time. Conclusion The radiotherapy schedule investigated in this study (i.e 34 Gy in 3.4 Gy/fr plus boost dose of 8 Gy in single fraction) is a feasible and safe treatment and does not lead to adjunctive acute and late toxicities. A longer follow up is expected to confirm these favourable results. Still, randomized prospective studies, designed to validate accelerated hypofractionated schedules, should be encouraged. References 1. Veronesi U, Marubini E, Mariani L, Galimberti V, Luini A, Veronesi P, Salvadori B, Zucali R: Radiotherapy after breast-conserving

surgery in small breast carcinoma. Long-term results of a randomized trial. Ann Oncol 2000, 12:997–1003.CrossRef 2. Fisher B, Anderson S, Bryant J, Margolese RG, Deutsch M, Fisher ER, Jeong JH, Wolmark N: Twenty-year follow-up of a randomized trial comparing total mastectomy, lumpectomy and lumpectomy plus irradiation for the treatment of invasive breast cancer. N Engl J Med 2002, 347:1233–1241.PubMedCrossRef 3. Early Breast Cancer Trialist’s Collaborative Group: Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: an overview of the randomised trials. Lancet 2005, 366:2087–2106. 4. Fowler JF: The linear-quadratic formula and progress in fractionated radiotherapy.

Our result suggested that PPARα agonist could sensitize the effect of NAC on cell growth inhibition and also implied that NAC may act as a potential PPARα ligand. Consistent with this, one report demonstrated a synergistic effect of PPARα agonist and NAC in control of brain tumor cells [18]. Note that no report showed a link between PPARα ligand and PDK1 although PDK1 was reported to be a target gene of PPARσ/β [19], another isoforms of PPAR family, which strongly expressed in the majority of lung cancers,

and Angiogenesis inhibitor activation of this isoform induced proliferation of lung cancer through pathways including activation of Akt phosphorylation correlated with up-regulation of PDK1 [20]. Note that the PDK1 promoter contains peroxisome proliferator responsive element (PPRE) [19], our data showed that PPARα ligand inhibited PDK1 promoter activity suggesting a distinct function of PPARα activation as compared to that of PPARσ/β. More studies are required to elucidate this. Furthermore, our results indicated that NAC–mediated downregulation of PDK1 reflected inhibition of transactivation of the PDK1 gene and also demonstrated that NAC, through activation of PPARα, increased tumor suppressor, p53 and reduced p65, a subunit of NF-κB, which played important roles in mediating the effect of NAC on inhibition of PDK1 expression. This again suggested the characteristic

of NAC acted as PPARα ligand. Silencing of p53 and overexprerssion of p65 blocked the effects of NAC on PDK1 expression further Liothyronine Sodium confirm the key roles of p53 and p65 in this process. P53 plays a critical role in tumor suppression mainly by inducing growth arrest, blocking

angiogenesis learn more and conferring the cancer cell sensitivity to chemoradiation [21]. Transcription factor NF-κB has been shown to regulate the expression of a number of genes that involve in many cellular processes such as inflammation and tumor growth [22]. Interestingly, the link of p53 in the regulation of glycolysis-dependent activation of NF-κB signaling in cancer has been reported [23]. However, the role of p53 and NF-κB in the direct regulation of PDK1 expression remains unknown. On the contrary, one study showed that overexpression of PDK1 resisted the apoptotic cell death caused by hypoxic injury and increased the expression of survival proteins, such as p53, in cultured rat cardiomyocytes [24]. Also, reports found that PDK1 plays a critical role by nucleating the T cell receptor-induced NF-κB activation pathway, which is important for T cell proliferation and activation during the adaptive immune response [25]. Together, these findings indicated that PDK1 was a critical regulator of tumor cell survival by modulating the p53 and NF-κB signaling pathways. NAC also had a direct or indirect effect on the regulation of p53 and NF-κB [26, 27]. The activation of p53 has been shown to mediate the effects of NAC on prostate cancer cell growth [28].

Table 1 Clinical characteristics of 60 patients   Total (n = 60) Age      Median, years 62.5    Range 38-84 Gender      Female 39 (65.0%)    Male 21 (35.0%) Smoking history      Nonsmoker 43 (71.7%)    Ex-smoker 11 (18.3%)    Current smoker 6 (10.0%) WHO Performance status      Normal activity 23 (38.3%) find more    Restricted activity 27 (45.0%)    In bed < 50% of the time 9 (15.0%)    In bed > 50% of the time 1 (1.7%) Tumor histology      ADC 53 (88.3%)    SQC 3 (5.0%)    LCC 1 (1.7%)    NSCLC NOS 2 (3.3%) Others 1 (1.7%) Stage      IIIA 3 (5.0%)    IIIB 4 (6.7%)    IV 53 (88.3%) Abbreviations: ADC adenocarcinoma, SQC squamous cell carcinoma, LCC large cell carcinoma,

NSCLC NOS non-small cell lung cancer not otherwise specified. Detection of EGFR mutations in plasma EGFR mutations were identified www.selleckchem.com/products/gsk1120212-jtp-74057.html in 10/60 (16.7%) plasma samples by PNA testing. Of these, seven (70.0%) were in-frame deletions within exon 19 and three (30.0%) were arginine-to-leucine substitutions at amino acid 858 in exon 21 (L858R) (Table 2). After 2 months of treatment, a repetition of the test in EGFR mutation-positive patients showed that none had EGFR mutations. Table 2 EGFR mutational status in plasma DNA samples   Positive Negative   EGFR mutation EGFR mutation   (n = 10) (n = 50) Exon 19 deletion 7 (70.0%) – Exon 21 point mutation 3 (30.0%) – Comparison of matched tumor sequencing and plasma EGFR mutations To evaluate the accuracy

of the results of the PNA test, we compared plasma EGFR mutations with tumor sequencing in 40 paired donor-matched plasma and tumor tissue specimens. EGFR mutations were detected in the plasma samples of six (15.0%) patients, including four deletions in exon 19 and two point mutations in exon 21. In the donor-matched tumor tissues, 35 mutations

were detected (87.5%) by using direct sequencing, including 18 in exon 19 and 17 in exon 21. Of the patients with plasma EGFR mutations, mutations of identical exon site were detected in the matched tumor tissues (Table 3). Wilson disease protein Table 3 EGFR mutational status in the paired specimens of plasma and tumor tissue N = 40 Plasma EGFR mutation     Positive Negative Tissue EGFR mutation positive 6 29   negative 0 5 Correlation between EGFR mutation status assessed by PNA-mediated real-time PCR clamping and clinical features EGFR mutations in plasma were detected more frequently in females (17.9% vs. 14.3% in male), non-smokers (18.6% vs. 11.8% in current/former smokers) and patients with stage IIIB disease (25.0% vs. 17.0% in stage IV). In addition, the overall mutation detection rate at the institute at which the central laboratory was located, and where sample processing did not require shipment, was relatively higher than that at the other institutes (23.8% vs. 12.8%); however, there were no statistically significant differences between the number of patients with EGFR mutations in plasma and those without (Table 4).

Therefore, larger and better-designed studies are required to overcome the limitations in the present study (particularly the information about Helicobacter pylori infection) and further confirm our observations. Acknowledgements This study was supported in part by National Institutes of Health grants R01 ES 11740-07 and CA 131274-01 (to Q. W.) and CA 16672 (to M. D. Anderson Cancer Center). We thank Margaret Lung and Kathryn Patterson for their assistance in recruiting the HTS assay subjects; Li-E Wang, Zhensheng Liu, Yawei Qiao, Min Zhao, Jianzhong He, and Kejin Xu for their laboratory assistance;

and Diane Hackett and Maude Veechfor for scientific editing. Electronic supplementary material Additional file 1: TGFB1 and VEGF genotype distributions and overall survival. The data provided represent the statistical analysis of TGFB1 and VEGF genotype distributions and overall this website survival. (DOC 69 KB) Additional file 2: TGFB1 and VEGF genotype distributions and 1-and 2-year survivals. The data provided represent the statistical analysis of TGFB1 and VEGF genotype distributions and 1-and 2-year survivals. (DOC 66 KB) References 1. Rohde H, Gebbensleben

B, Bauer P, Stutzer H, Zieschang J: Has there been any improvement in the staging of gastric cancer? Findings from the German Gastric Cancer TNM Study Group. Cancer 1989, 64: 2465–2481.CrossRefPubMed 2. Catalano V, Labianca R, Beretta GD, Gatta G, de Braud F, Van Cutsem E: Gastric cancer. Crit Rev Oncol Hematol 2009, in press. 3. Becker KF, Keller G, Hoefler H: The use of molecular biology in diagnosis and prognosis of gastric cancer. Surg Oncol 2000, 9: 5–11.CrossRefPubMed 4. Wu GY, Hasenberg T, Magdeburg R, Bonninghoff R, Sturm JW, Keese M: Association between EGF, TGF-beta1, VEGF gene polymorphism and colorectal

cancer. World J Surg 2009, 33: 124–129.CrossRefPubMed 5. Li T, Cao BW, Dai Y, Cui H, Yang HL, Xu CQ: Correlation of transforming growth factor beta-1 gene polymorphisms C-509T and T869C Methane monooxygenase and the risk of gastric cancer in China. J Gastroenterol Hepatol 2008, 23: 638–642.CrossRefPubMed 6. Liu DH, Zhang XY, Fan DM, Huang YX, Zhang JS, Huang WQ, Zhang YQ, Huang QS, Ma WY, Chai YB, Jin M: Expression of vascular endothelial growth factor and its role in oncogenesis of human gastric carcinoma. World J Gastroenterol 2001, 7: 500–505.PubMed 7. Watson CJ, Webb NJ, Bottomley MJ, Brenchley PE: Identification of polymorphisms within the vascular endothelial growth factor (VEGF) gene: correlation with variation in VEGF protein production. Cytokine 2000, 12: 1232–1235.CrossRefPubMed 8. Renner W, Kotschan S, Hoffmann C, Obermayer-Pietsch B, Pilger E: A common 936 C/T mutation in the gene for vascular endothelial growth factor is associated with vascular endothelial growth factor plasma levels. J Vasc Res 2000, 37: 443–448.CrossRefPubMed 9.

8–40.1 1861.1130 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Glu Gln Lxxol 61 40.9–41.0 1874.1420 Ac Aib Ala Aib Ala Vxx Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Gln Gln Lxxol 62 41.5–41.6 1875.1390 Ac Aib Ala Aib Aib Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Glu Gln Lxxol 63 41.9–42.0 1875.1284 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Lxx Aib Vxx Glu Gln

Lxxol No. Compound identical or positionally isomeric with Ref.                                         56 Minutisporin-1 (pos. 1–3, 6, 7, 11–16, 18 and 19: cf. trichostrigocins A and B) Degenkolb et al. 2006a                                   57 Minutisporin-2 (cf. hypophellin-18: [Pheol]19 → [Lxxol]19; pos 1, 6, 7, 9, and the C-terminal nonapeptide: AZD4547 clinical trial tricholongin B-I) Rebuffat et al. 1991                                   58 Minutisporin-3 (cf. hypophellin-19: [Pheol]19 → [Lxxol]19; trichosporin B-IIIb – [Aib]6, [Pheol]19 → [Lxxol]19) Röhrich et al. 2013a, Nutlin-3 b; Iida et al. 1990                                   59 Minutisporin-4 (cf. hypophellin-20: [Pheol]19 → [Lxxol]19; cf. trichosporin B-VIa – [Aib]6, [Aib]16 → [Vxx]16, [Pheol]19 → [Lxxol]19; C-terminal nonapeptide, cf. tricholongin B-II; cf.

trichocellin A-5 – [Ala]6, [Pheol]20 → [Lxxol]20) Rebuffat et al. 1991; Wada et al. 1994                                   60 Minutisporin-5 (C-terminal octapeptide, cf. hypelcin B-III) Matsuura et al. 1994                                   61 Minutisporin-6 (cf. hypophellin-22: [Pheol]19 → [Lxxol]19; trichorzin HA-V: [Vxx]5–[Pro]13 and C-terminus with [Lxx]14 → [Vxx]14) Hlimi et al. 1995; Röhrich et al. 2013a                                   62 Minutisporin-7                                           63 Minutisporin-8        

                    Suplatast tosilate               aVariable residues are underlined in the table header. Minor sequence variants are underlined in the sequences. This applies to all sequence tables Table 11 Sequences of 19-residue peptaibiotics detected in the plate culture of Hypocrea minutispora No. tR [min] [M + H]+   Residuea 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 64 36.1–36.3 1832.1060 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Aib Gln Gln Vxxol 65 37.3–37.5 1832.1025 Ac Aib Ala Aib Gly Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Gln Gln Vxxol 66 37.5–37.9 1846.1196 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Vxx Aib Pro Vxx Aib Vxx Gln Gln Lxxol 57 37.8–38.0 1846.1199 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Aib Gln Gln Lxxol 67 38.6–38.7 1847.1135 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Aib Glu Gln Lxxol 59 39.0–39.2 1860.1318 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Gln Gln Lxxol 60 39.8–40.0 1861.1271 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Vxx Aib Vxx Glu Gln Lxxol 68 40.4–40.6 1874.1492 Ac Aib Ala Aib Ala Aib Gln Aib Lxx Aib Gly Lxx Aib Pro Lxx Aib Vxx Gln Gln Lxxol 61 40.6–40.9 1874.

For the purpose of tracking the uptake of micelles by macrophages, QDs were incorporated into find more the micelle preparations because of its extreme brightness and photostability in real time imaging. Furthermore, QDs can be substituted by other inorganic nanoparticles such as gadolinium, iron oxide, gold, and tantalum for clinical translation. The PS micelles were further assembled with an amphiphilic polymeric surfactant, phospholipid conjugated to polyethylene glycol (PL-PEG) for the solubilization of hydrophobic nanoparticles (QD), improved dispersibility of micelles

in physiological buffers and prolonged circulation in vivo [14]. However, PEGylation can potentially interfere with the interactions between ligand and cell surface receptor and reduce cellular uptake [17, 18], a fine balance between stability and targeting for PEGylated nanoparticles were extensively studied. We hypothesize that the ratio of PL-PEG and PS shell coverage for 6- to 8-nm hydrophobic trioctylphosphine oxide (TOPO) quantum dot (QD) could be optimized for colloidal stability and targeting efficacy. Methods Materials L-α-phosphatidylserine MK-8669 in vitro (PS), 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy (polyethylene glycol)-2000] (ammonium salt) (DSPE-mPEG, 2kDa) were purchased from Avanti Polar Lipids, Inc. (Alabaster, AL, USA). All other chemicals were obtained from Sigma-Aldrich Corporation (St. Louis,

MO, USA). Dulbecco’s modified Eagle’s medium (DMEM), fetal bovine serum (FBS), phosphate-buffered saline (PBS), penicillin-streptomycin, Montelukast Sodium and hydrophobic

trioctylphosphine oxide (TOPO) QDs (QD 620nm) were purchased from Ocean Nanotech, Corp (Carlsbad, CA, USA). MTT assay kit was purchased from Roche Applied Science (Indianapolis, IN, USA). Lab-TekTM chamber slide system was purchased from Thermo Scientific/Nalgene Nunc International (Rochester, NY, USA). Vectashield mounting medium with DAPI was purchased from Vector Laboratories, Inc. (Burlingame, CA, USA). J774A.1 monocytic cell line was obtained from American Type Cell line Collection (ATCC) (ATCC® TIB67™). A 100-kD dialysis membrane was purchased from Spectrum Laboratories (Irvine, CA, USA). Preparation of PS-QD micelles Micelles were prepared by the addition of hydrophobic QDs in chloroform to phospholipids (PLs) at each mole ratio (PEG/PS 100:0, 60:40, 50:50, 40:60, and 0:100) in hot water under vigorous stirring, followed by high-speed homogenization to form a uniform milky micro-emulsion. Unless otherwise mentioned, only PS mole ratio is shown and the remaining assumed for PL-PEG mole ratio (for example, PS (0) means micelles made entirely from phospholipid methoxy PEG, PS (40) means PS/PL-PEG mole ratio is 60:40). Briefly, the PLs at various mole ratios as indicated in Table 1 were first dissolved in water at 50°C and QD 620 (0.2 nmol) dissolved in chloroform was added to PLs in water and briefly sonicated for a few minutes.

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