Walking capacities in multiple sclerosis measured by global posit

Walking capacities in multiple sclerosis measured by global positioning system odometer. Mult Scler. 2007;13(2):220–3.PubMedCrossRef 41. Fahey MC, Corben LA, Collins

V, Churchyard AJ, Delatycki MB. The 25-foot walk velocity accurately measures real world ambulation in Friedreich ataxia. Neurology. 2007;68(9):705–6.PubMedCrossRef 42. Coleman CI, Sobieraj DM, Marinucci LN. Minimally important clinical difference of the Timed 25-Foot Walk Test: results from a randomized controlled trial in patients with multiple sclerosis. Curr Med Res Opin. 2012;28(1):49–56. doi:10.​1185/​03007995.​2011.​639752.PubMedCrossRef 43. Kaufman M, Moyer D, Norton J. The significant change for the Timed 25-foot Walk in the multiple sclerosis functional composite. Mult Scler. 2000;6(4):286–90.PubMed 44. Schwid SR, Goodman AD, McDermott MP, Bever CF, Cook AZ 628 SD. Quantitative functional measures in MS: what is a reliable change? Neurology. 2002;58(8):1294–6.PubMedCrossRef 45. Beninato M, Gill-Body KM, Salles S, Stark PC, Black-Schaffer Autophagy inhibitor RM, Stein J. Determination of the minimal clinically important difference in the FIM instrument in patients with stroke. Arch Phys Med Rehabil. 2006;87(1):32–9.PubMedCrossRef”
“1 Introduction Doxylamine succinate, an ethanolamine-based antihistamine, shares the actions and uses of other antihistamines. Because of its sedative effect, doxylamine medicinal products (alone or in combination with other drugs) have been authorized for more

than 50 years with an appropriate extent of use for short-term management of insomnia [1–5]. Currently, it is a medical product with a legal base of well-established use in Europe. Based on clinical practice, the recommended adult dose for doxylamine hydrogen succinate as a nighttime sleep aid is 25 mg, once daily, taken orally up to half an hour before bedtime. If drowsiness is excessive, the dosage should be reduced to 12.5 mg. Doses higher than 25 mg are not recommended. Dormidina® has been marketed in Spain since 1990 with a unique active ingredient: doxylamine hydrogen succinate, 12.5 mg or 25 mg. Because its marketing authorization was Belnacasan in vitro approved before the implementation of the oxyclozanide present regulatory

standards, a new pharmacokinetic study of doxylamine hydrogen succinate in its current pharmaceutical presentation (film-coated tablets) has been recently published [6]. This study provides updated data on the pharmacokinetic parameters of doxylamine following a 25 mg dose in both fasting and fed conditions. The results indicate that the kinetic parameters of doxylamine were not affected by a high-fat, high-calorie food intake, and the drug was safe and well tolerated by the subjects. Furthermore, no differences between genders were observed [6]. No data on the dose proportionality of doxylamine were available. Therefore, the main objective of this study was to evaluate and compare the bioavailability with regard to dose proportionality between the two marketed strengths (12.

J Gerontol A Biol Sci Med Sci 62:440–446PubMed 22 Mowe M, Haug E

J Gerontol A Biol Sci Med Sci 62:440–446PubMed 22. Mowe M, Haug E, Bohmer T (1999) Low serum calcidiol concentration in older adults with reduced muscular function. J Am Geriatr Soc 47:220–226PubMed 23. Plotnikoff GA, Quigley JM (2003) Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 78:1463–1470CrossRefPubMed 24. Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA (2003) Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc 51:1762–1767CrossRefPubMed 25. Verreault R, Semba RD, Volpato

S, Ferrucci L, Fried LP, Guralnik JM (2002) Low serum vitamin D does not predict new disability or loss of muscle strength in older women. J Am Geriatr Soc 50:912–917CrossRefPubMed 26. www.selleckchem.com/products/Fludarabine(Fludara).html Stel VS, Smit JH, Pluijm SMF, Lips P (2003) Balance and mobility performance as treatable risk factors for recurrent falling in older persons. J Clin Epidemiol 56(7):659–668CrossRefPubMed 27. Pluijm SMF, Tromp AM, Smit JH, Deeg DJH, Lips P (2000) Consequences of vertebral deformities in older men and women. J Bone Miner Res 15:1564–1572CrossRefPubMed 28. Rasbash J, Steele F, Browne W, Prosser B (2005) A user’s guide to MLwiN. Version 2.0. University of Bristol,

Bristol 29. Maas CJM, Snijders TAB (2003) The multilevel approach to repeated measures for complete and BCKDHA incomplete data. IWR-1 in vitro Quality & Quantity 71−89 30. Snijders TAB, Bosker RJ (1999) Multilevel analysis. An introduction to basic and advanced multilevel modeling. Sage, London 31. Chel VG, Ooms ME,

Popp-Snijders C, Pavel S, Schothorst AA, Meulemans CC, Lips P (1998) Ultraviolet irradiation corrects vitamin D deficiency and suppresses secondary hyperparathyroidism in the elderly. J Bone Miner Res 13:1238–1242CrossRefPubMed 32. Binkley N, Novotny R, Krueger D, Kawahara Y, Daida YG, Lensmeyer B, Hollis BW, Drezner MK (2007) Low vitamin D status despite abundant sun exposure. J Clin Endocrinol Metab 92:2130–2135CrossRefPubMed 33. Chel V, Wijnhoven HA, Smit JH, Ooms ME, Lips P (2008) Efficacy of different doses and time intervals of oral vitamin D supplementation without calcium in elderly nursing home residents. Osteoporosis Int 19:663–671CrossRef 34. Snijder MB, van Dam RM, Visser M, Deeg DJ, Dekker JM, Bouter LM, Seidell JC, Lips P (2005) Adiposity in selleck relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab 90:4119–4123CrossRefPubMed 35. Greig CA, Young A, Skelton DA, Pippet E, Butler FM, Mahmud SM (1994) Exercise studies with elderly volunteers. Age Ageing 23:185–189CrossRefPubMed 36. Kallman DA, Plato CC, Tobin JD (1990) The role of muscle loss in the age-related decline of grip strength: cross-sectional and longitudinal perspectives. J Gerontol 45:M82–M88PubMed 37.

, with some modification [8] Briefly, PHELP DNA was amplified wi

, with some modification [8]. Briefly, PHELP DNA was amplified with the primer pair PhelpFsoe(LI)/PhelpRsoe from the plasmid pPL2luxPHelp [16] and fused between two DNA fragments amplified from the regions flanking P llsA by splicing by overlap extension (SOE) PCR [17]. The upstream region was amplified with the primer pair PllsAchgA(LI) and PllsAchgB(LI) and the downstream region was amplified with primers PllsAchgC and PllsAchgD. All PCRs were performed using Vent DNA polymerase (NEB, New England AZD2281 manufacturer Biolabs, MA, USA). The SOE PCR product was cloned into the multiple cloning site (MCS) of check details pORI280 following

PstI and EcoRI (NEB) digestion and ligation with the Ligafast rapid DNA ligation system (Promega, Madison, USA). The sequence of the cloned product was verified with MCS primers pORI280For/Rev by MWG Biotech, Germany [18]. Pellet-paint (Novagen) precipitated plasmid was subsequently transformed into the intermediate repA-positive host E. coli EC101. The plasmid was co-transformed into L. innocua FH2051 with the highly temperature-sensitive plasmid pVE6007 which supplies RepA in trans. Transformed cells appeared as blue colonies following plating on BHI-Ery-Xgal AZD8931 mouse at 30°C. The integration of pORI280 by single crossover homologous recombination was stimulated by picking a single blue colony from the transformation plate and incubating it on BHI-Ery-Xgal at 30°C for 24 h and subcultured

twice on BHI-Ery-Xgal at 42°C. A second crossover event, resulting in the introduction of PHELP Docetaxel nmr in place of PllsA and the eventual loss of the pORI280 vector, was screened for following multiple subcultures in the absence of antibiotic selection. The introduction of PHELP upstream of llsA in Ery resistant Cm sensitive colonies was confirmed by PCR. A haemolytic phenotype

was determined by spotting 10 μL of an overnight culture of this strain onto Columbia blood agar (Oxoid) containing 5% defibrinated horse blood (TCS Biosciences, Buckingham, UK) and 1 mU/ml sphingomyelinase (Sigma) and examining after 24 h. Pulsed- field gel electrophoresis Pulsed-field gel electrophoresis was carried out following the CDC standardized PulseNet protocol for L. monocytogenes with AscI and ApaI as the restriction endonucleases. The PFGE patterns were analyzed using BioNumerics software [19]. Results and discussion Screening L. monocytogenes and L. innocua for homologues of llsA To date LIPI-3 has been identified in ~60% (27 of 46) of lineage I L. monocytogenes but was absent from all lineage II (n = 23) and lineage III (n = 5) isolates tested [8]. As a consequence of gaining access to the Seeliger collection of Listeria isolates [20], we were provided with the opportunity to screen for the presence of LIPI-3 among an additional 83 L. monocytogenes isolates including 30 lineage I, 50 lineage II and 3 lineage III strains. The llsA gene was not identified in any lineage II or lineage III strain, consistent with our previous observations (Table  1).

46) to the Kauffmann-White scheme Res Microbiol 2004, 155:568–57

46) to the Kauffmann-White MDV3100 scheme. Res Microbiol 2004, 155:568–570.CrossRefPubMed PP2 10. Alcaine SD, Soyer Y, Warnick

LD, Su WL, Sukhnanand S, Richards J, Fortes ED, McDonough P, Root TP, Dumas NB, et al.: Multilocus sequence typing supports the hypothesis that cow- and human-associated Salmonella isolates represent distinct and overlapping populations. Appl Environ Microbiol 2006, 72:7575–7585.CrossRefPubMed 11. Alcaine SD, Sukhnanand SS, Warnick LD, Su WL, McGann P, McDonough P, Wiedmann M: Ceftiofur-resistant Salmonella strains isolated from dairy farms represent multiple widely distributed subtypes that evolved by independent horizontal gene transfer. Antimicrob Agents Chemother 2005, 49:4061–4067.CrossRefPubMed 12. Sukhnanand S, Alcaine S, Warnick LD, Su WL, Hof J, Craver MP, McDonough P, Boor KJ, Wiedmann M: DNA sequence-based IACS-10759 mw subtyping and evolutionary analysis of selected Salmonella enterica serotypes. J Clin Microbiol 2005, 43:3688–3698.CrossRefPubMed 13. Harbottle H, White DG, McDermott

PF, Walker RD, Zhao S: Comparison of multilocus sequence typing, pulsed-field gel electrophoresis, and antimicrobial susceptibility typing for characterization of Salmonella enterica serotype Newport isolates. J Clin Microbiol 2006, 44:2449–2457.CrossRefPubMed 14. Baumler AJ, Tsolis RM, Ficht TA, Adams LG: Evolution of host adaptation in Salmonella enterica. Infect Immun 1998, 66:4579–4587.PubMed 15. Kingsley RA, Baumler AJ: Host adaptation and the emergence of infectious disease: the Salmonella paradigm. Mol Microbiol 2000, 36:1006–1014.CrossRefPubMed

16. Rabsch W, Andrews HL, Kingsley RA, Prager R, Tschape H, Adams LG, Baumler AJ:Salmonella enterica serotype Typhimurium and its host-adapted variants. Infect Immun 2002, 70:2249–2255.CrossRefPubMed 17. Maiden MC, Bygraves JA, Feil E, Morelli G, Russell JE, Urwin R, Zhang Q, Zhou J, Zurth K, Caugant DA, et al.: Multilocus sequence typing: a portable approach to the identification of clones within populations of pathogenic microorganisms. Proc Natl Acad Sci USA 1998, 95:3140–3145.CrossRefPubMed 18. Guerra B, Vasopressin Receptor Junker E, Miko A, Helmuth R, Mendoza MC: Characterization and localization of drug resistance determinants in multidrug-resistant, integron-carrying Salmonella enterica serotype Typhimurium strains. Microb Drug Resist 2004, 10:83–91.CrossRefPubMed 19. Chu C, Chiu CH: Evolution of the virulence plasmids of non-typhoid Salmonella and its association with antimicrobial resistance. Microbes Infect 2006, 8:1931–1936.CrossRefPubMed 20. Gulig PA, Danbara H, Guiney DG, Lax AJ, Norel F, Rhen M: Molecular analysis of spv virulence genes of the Salmonella virulence plasmids. Mol Microbiol 1993, 7:825–830.CrossRefPubMed 21.

The primary mechanism of fusidic acid resistance in S aureus rel

The primary mechanism of fusidic acid resistance in S. aureus relates to mutations in fusA, the gene that encodes the ribosomal translocase and translation elongation LCZ696 factor EF-G [12, 13]. More than 30 different amino acid substitution mutations in fusA have been identified [12, 14, 15]. Subsequently, resistance in natural isolates may also result from the horizontal acquisition of fusB, a poorly

characterized plasmid-mediated resistance mechanism [13]. The gene fusB is usually carried by a 21-kb plasmid, pUB101 [16], however, it can also be chromosomal [17]. The fusB gene encodes an inducible protein that protects an in vitro translation system against the inhibitory action of fusidic acid [8]. Recently, two fusB homologues, designated fusC and fusD, have been identified in the chromosome of clinical isolates of S. aureus and S. saprophyticus, respectively [18]. In addition, fusidic acid-resistant small-colony variants (SCVs) of S. aureus with mutations in rplF have been designated as FusE mutants [14]. Although frequencies of resistance to fusidic acid have remained generally low, each of these mechanisms has multiple genetic causes, and

emerging resistance is a problem that could limit the therapeutic options available for treatment of staphylococcal infections [19]. In this study, a series of MRSA clinical isolates recovered at a regional teaching hospital in middle Taiwan showing fusidic acid MIC ≥ 2 μg/ml. The high distribution check details of fusidic acid resistance determinants fusC was confirmed in MRSA. In addition, different fusidic acid resistance determinants-containing in one isolate was also this website demonstrated. Methods Bacterial isolates From April 2007 to January 2008, 34 clinical isolates of MRSA with fusidic acid resistance were recovered from 34 different patients MG-132 cell line at Tungs’ Taichung MetroHarbor Hospital (TTMHH), a 1405-bed regional teaching hospital in central Taiwan. S. aureus ATCC 29213 and NCTC 8325 have consistently been used as a quality control strain and Pulsed Field Gel Electrophoresis (PFGE) standard strain, respectively. Luria-Bertani (LB) agar and LB broth were used for bacterial growth

at 37°C with aeration. Mueller-Hinton agar was used for all determinations of minimum inhibitory concentrations (MICs). All isolates were identified on the colony morphology, Gram’s stain, a positive catalase reaction and/or results obtained with the phoenix system (BD Diagnostic Systems, Sparks, MD, USA) and frozen at -80°C until used. Antimicrobial susceptibility tests MICs of different antimicrobial agents were determined using the Phoenix Automated Microbiology System (BD Diagnostic Systems, Sparks, MD) and interpreted according to the criteria provided by the Clinical and Laboratory Standards Institute (CLSI). Fusidic acid susceptibility was screened by the disk diffusion method with 10 μg fusidic acid containing disks. The interpretive criterion of susceptibility was an inhibition zone ≥ 22 mm in diameter.

In addition of medical records reviewing, these patients were inv

In addition of medical records reviewing, these patients were invited to entry in a follow-up research protocol. The post-trauma follow-up goals were: 1) to clinically evaluate patients, regarding complaints, past medical history, family history, and findings in the physical examination, 2) to evaluate kidney morphology and the renal blood flow by means of computed tomography of abdomen and MRA, 3) to evaluate renal function by using DMSA renal scintigraphy to detect and quantify differences

in renal function, 4) to evaluate the incidence of arterial hypertension in the follow-up of these cases by using ambulatory blood-pressure monitoring, 5) to evaluate if anatomical and functional kidneys alterations in association with arterial selleck products GDC-0973 manufacturer hypertension correlate with the grade of renal trauma, defined by CT, at the patient’s admission and 6) when hypertension were present, to investigate possible renal vascular etiology by dynamic 99mtechnetium ethylenedicysteine (99mTc EC) renal scintigraphy, using the captopril-stimulated study. For laboratory

evaluation, all patients of the study had: serum levels of urea and creatinine, electrolytes (sodium, potassium and calcium), total protein, albumin, lipidogram (cholesterol, LDL, HDL and triglycerides), hemoglobin, hematocrit, fasting glycemia and urine analysis. Abdominal CT scans were PI3K signaling pathway performed also, to detect and monitor complete resolution of perinephric hematoma and urinoma, when present. Magnetic resonance were performed on a 1.5 Tesla scanner, Magneton Vision, from Siemens (Erlangen – Germany), with a dedicate torso coil. We employed sequences to evaluate renal morphology and the status of major renal arteries. Our MG-132 cell line protocol includes images weighted in T1 and T2, on axial and coronal planes, using Gradient-Echo and Turbo Spin-Echo sequences. For MRA, we used the “bolus test” technique to set the ideal time for the arterial phase. A 3D-Gradient-Eco sequence was applied along the coronal plane for angiography (Repetition Time = 4.6 ms and

Echo Time =1.8 ms, flip angle of 25 degrees and 1.0 mm slice thickness). Images were processed at a Siemens workstation using Maximum Intensity Projection (MIP) and Multiplanar Reformatting (MPR) techniques for angiography. Flow quantification was performed using phase-contrast sequence (TR = 24.0 ms, TE = 5.0 ms, Flip Angle = 30) with cardiac and respiratory gating. Flow measurements were also performed at the same workstation using the software Flow Quantification provided by Siemens Medical Systems. Peak systolic velocity and acceleration time were the additional hemodynamic parameters evaluated. Quantitative DMSA scintigraphy was performed in all patients. Differential renal function was calculated by adding the individual counts of both kidneys and recording the fractional contribution of each kidney as a percentage of total renal function.

Norrby S, Nord CE, Finch R: Lack of development of new antimicrob

Norrby S, Nord CE, Finch R: Lack of development of new antimicrobial drugs: a potential serious threat to public health. Lancet Infect Dis 2005, 5:115–9.PubMed 3. Lehrer RI, Ganz T: Cathelicidins: a family of endogenous antimicrobial peptides. Curr Opin Hematol 2002, 9:18–22.PubMedCrossRef 4. Lehrer RI: Primate defensins. Nature Rev Microbiol 2004, 2:727–738.CrossRef 5. Yang D, Biragyn A, Hoover DM, Lubkowski J, Oppenheim JJ: Multiple roles of antimicrobial defensins, cathelicidins, and eosinophil-derived neurotoxin in host defense. Annu Rev Immunol 2004, buy Tariquidar 22:181–215.PubMedCrossRef 6. Mygind PH, Fischer RL, et al.: Plectasin is a peptide antibiotic with therapeutic potential from a saprophytic fungus. Nature 2005, 437:975–80.PubMedCrossRef

7. Gottlieb CT, Thomsen LE, Ingmer H, Mygind PH, Kristensen H-H, Gram L: Antimicrobial peptides effectively kill a broad spectrum of Listeria monoc ytogenes and Staphylococcus aureus strains independently of origin, sub-type, or virulence factor expression. BMC Microbiol

2008, 8:205.PubMedCrossRef 8. Waldvogel FA: Staphylococcus aureus . In Principles and practice of infectious diseases. Edited by: Mandell GL, Bennet JE, Dolio R. New York: Churchill Livingstone; 1995:1754–1777. 9. Vazquez-Boland SC79 JA, Kuhn M, Berche P, Chakraborty T, Dominguez-Bernal G, Goebel W, Gonzalez-Zorn B, Wehland J, Kreft J: Listeria Pathogenesis and Molecular Virulence Determinants. Clin Microbiol Rev 2001, 14:584–640.PubMedCrossRef 10. Brogden KA: Antimicrobial peptides: pore formers or metabolic inhibitors in bacteria. Nat Rev Microbiol 2005, 3:238–250.PubMedCrossRef Fossariinae 11. Ando T, Watanabe S: A new method for fractionation of protamines and amino acid sequences of salmine and 3 components of iridine. Int J Protein Res 1969, 1:221–224.PubMedCrossRef 12. Schneider T, Kruse T, Wimmer R, et al.: Plectasin, a fungal defensin, targets the bacterial cell wall precursor Lipid II. Science 2010, 328:1168–1172.PubMedCrossRef 13. Hale JD, Hancook RE: Alternative mechanisms of action of cationic antimicrobial peptides on bacteria. Expert

rec Anti Inf Ther 2007, 5:951.CrossRef 14. Torres VJ, Stauff DL, Pishchany G, Bezbradica JS, Gordy LE, Iturregui J, Anderson KL, Dunman PM, Joyce S, Skaar EP: A Staphylococcus aureus regulatory system that Temsirolimus responds to host heme and modulates virulence. Cell Host microbe 2007, 1:109–119.PubMedCrossRef 15. Everse J, Hsia N: The toxicities of native and modified hemoglobins. Free Radic Biol Med 1997, 22:1075–1099.PubMedCrossRef 16. Stauff DL, Torres VJ, Skaar EP: Signaling and DNA-binding activities of the Staphylococcus aureus HssR-HssS two-component system required for heme sensing. J Biol Chem 2007, 282:26111–26121.PubMedCrossRef 17. Stauff DL, Bagaley D, Torres VJ, Joyce R, Anderson KL, Kuechenmeister L, Dunman PM, Skaar EP: S taphylococcus aureus HrtA is an ATPase required for protection against heme toxicity and prevention of a transcriptional heme stress response. J Bacteriol 2008, 190:3588–3596.

The effects of LS081 on ferritin expression were determined under

The effects of LS081 on ferritin expression were determined under two conditions: RPMI1640-10% FCS to which 2 μM ferric ammonium citrate was added or RPMI with 10% iron saturated FCS. As shown in Figure 2, LS081 at 3 and 10 μM stimulated ferritin synthesis from both ferric ammonium citrate and iron saturated Tf. In preliminary

experiments the level of ferritin protein was not significantly increased by compound alone (data not shown). Figure 2 The effect of LS081 on ferritin expression. PC-3 cells were treated for 16 hr with DMSO alone, or 3 or 10 μM LS081 in the presence of non-transferrin-bound-iron selleck products (ferric ammonium citrate, left panel) or transferrin-bound-iron (Fe-saturated-Tf, right panel). The cellular proteins were separated by SDS-PAGE, and ferritin heavy chain, and β-actin detected by Western blotting as described Pitavastatin in the Methods. The top panel shows a representative autoradiography. The bottom panel shows the ratio of ferritin to the actin loading control by densitometric analysis (mean values ± SEM of 3-4 separate experiments). *: p < 0.05, **: p < 0.01 compared

to DMSO alone by 1-way ANOVA with Tukey’s posttests. Iron LCZ696 facilitation is cytotoxic to cancer cells We examined the effect of the iron facilitator LS081 on ROS generation using DCFDA whose fluorescence intensity is increased in response to elevated intracellular ROS. As shown in Figure 3, K562 cells had significantly increased levels of ROS production when exposed to LS081 in the presence of ferric ammonium citrate but not with iron or LS081 alone. Figure 3 The effect of LS081 on ROS generation. Approximately 5 × 105 K562 cells were treated for 30 min with 0.1% DMSO alone, 10 μM ferric ammonium citrate alone, 3 or 10 μM LS081 alone, or the combination of Fe and LS081 at the indicated concentrations. The cells were then incubated with DCFDA and fluorescence measured by a BD Calibur Flow cytometer expressing the fluorescence as the mean total fluorescence intensity in the gated area. Shown are the means ± SEM of 3 separate

experiments with 2-3 replicates for each experiment. *** denotes P < 0.001 compared to the DMSO, Fe, or LS081 alone by 1-way ANOVA with Tukey's Non-specific serine/threonine protein kinase posttests. The proliferation of PC-3 cells, a prostate cancer cell line, was not inhibited by 10 μM ferric ammonium citrate or 10 μM LS081 when cultured in 10% FCS-RPMI1640 for 24 or 48 hrs (Table 1) or 72 hr (data not shown). However, as also shown in Table 1, treatment with 10 μM LS081 plus 10 μM ferric ammonium citrate for 24 hr or 48 hr significantly reduced the number of cells relative to controls. When grown in serum-free medium (Figure 4), 267B1 cells, an immortalized, non-malignant prostate cell line, showed slight growth inhibition with 3 or 10 μM LS081 alone with no potentiation of growth inhibition by the addition of 2 μM ferric ammonium citrate.

Adv Drug Delivery Rev 2011, 63:730–747 CrossRef 25 Lvov Y, Deche

Adv Drug Delivery Rev 2011, 63:730–747.CrossRef 25. Lvov Y, Decher G, Moehwald H: Assembly, structural characterization, and thermal behavior of layer-by-layer deposited ultrathin films of poly (vinyl sulfate) and poly (allylamine). Langmuir 1993, 9:481–486.CrossRef 26. Aliev FG, Correa-Duarte MA, Mamedov A, Ostrander JW, Giersig M, Liz-Marzán LM, Kotov NA: Layer-by-layer assembly of core-shell magnetite nanoparticles: effect of silica coating on interparticle interactions and magnetic properties. Adv Mater 1999, 11:1006–1010.CrossRef 27. Yang Y-J, Tao X, Hou Q,

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Cancer Res 2006, 66:3639–3648 PubMedCrossRef 11 Gaustad JV, Simo

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