NN and MA were supported by the Swiss National Science Foundation

NN and MA were supported by the Swiss National Science Foundation grant 31003A_130735. Electronic supplementary material Additional file 1: File S1: Flow cytometry data. (XLS 137 KB) Additional SHP099 solubility dmso file 2: Figure S1: Variation in the expression of ptsG, mglB and rpsM reporters across different environments. The CV of log expression of PptsG-gfp (green), PmglB-gfp (blue) and PrpsM-gfp (red) was plotted against the mean log expression. Power regression was fitted to each dataset corresponding to the expression

of the same reporter across different environments. The individual curves of variation in the expression of ptsG and rpsM reporters showed negative associations between the mean expression and the

variation of expression across environments, whereas the mglB reporter showed a positive association. (TIFF 145 KB) Additional file 3: Text S1: Analysis of expression of fluorescent reporters in glucose-acetate mixtures. (PDF 57 KB) Additional file 4: Figure S2: Reporter expression in mixed-substrate environments. Expression of ptsG, mglB and acs reporters was measured in chemostats (D = 0.15 h-1) in mixed-substrate environments supplemented with 0.28 mM Glc and 0.28 mM Ac (green), or 2.8 mM Glc and 2.8 mM Ac (blue). The distributions were plotted together with the measurements of the reporter expression in the environments GDC-0449 mouse with only glucose in the feed (0.56 mM Glc – orange, and 5.6 mM

Glc – red). The fluorescence of the promoterless strain is presented in black. (TIFF 544 KB) Additional file 5: Figure S3: Expression of the pck reporter in different chemostat and batch conditions. Ppck-gfp fluorescence (indication of flux to gluconeogenesis) was measured in bacterial populations grown in chemostats (D = 0.15 h-1) and batch environments supplied with minimal media supplemented with only D-glucose, only sodium acetate or D-glucose plus sodium acetate. Again, background fluorescence is the fluorescence of the promoterless strain, depicted in black. The expression of the pck reporter was decreased in the exponential phase in glucose batch cultures in comparison PD184352 (CI-1040) to carbon-limited chemostats. (TIFF 757 KB) Additional file 6: Figure S4: Changes in gfp expression prior of reaching theoretical steady-state. Pacs-gfp fluorescence was measured for five independent replicates growing on different concentration of glucose in the feed. At time point of 0 hours, chemostat experiments were started at a minimal dilution rate of D = 0.14 h-1. After 24 hours, dilution rates were increased to D = 0.15 h-1. The fluorescence plots show gfp distribution in bacterial populations without gating, together with fluorescence of the promoterless strain depicted in black. All independent replicates showed reproducible measurements of GFP fluorescence after 3.6 volume turnovers at D = 0.15 h-1.

​tcdb ​org a Transporter classes 6 and 7 have not been assigned

​tcdb.​org. a Transporter classes 6 and 7 have not been assigned in the TC system yet and therefore are

not listed here. b Auxiliary proteins facilitate transport via established transport systems and therefore are not counted as a separate system. Of the channel proteins, almost all are alpha-type channels (Subclass 1.A). A few outer membrane porins (Subclass 1.B) were identified, but these were not examined more closely because of the recent extensive studies of Bhat et al. [33]. No potential channel-forming toxins (Subclass 1.C) were detected. The secondary carriers include mostly symporters (importers) and antiporters selleck chemical (exporters), while almost all primary active transporters are ATP-dependent (Subclass 3.A). However, a smaller percentage may be oxidoreduction driven (Subclass 3.D) or decarboxylation driven (Subclass 3.B). Among the seven group translocation proteins, two belong to the phosphotransferase system (Subclass 4.A), while five may be acyl CoA ligase-coupled transport systems (Subclass 4.C). Of the ten proteins possibly functioning as transmembrane electron flow carriers, all ten are likely to carry an electron pair (Subclass 5.A). None is likely to be a single electron carrier (Subclass 5.B). Eight auxiliary transport proteins (Subclass 8.A)

and ten recognized transporters of unknown mechanism of action (Subclass 9.A) were also identified. Substrates transported by Mxa Table 5 and Figure 5 show numbers of transport proteins Pyruvate dehydrogenase in Sco organized according to substrate types. Transporters that utilize inorganic molecules as substrates make up a large portion of all click here transport proteins found in Mxa. Cation-specific transporters (23.7% — 84 total) are split evenly between primary and secondary carrier

systems (36 and 38 proteins, respectively) with only six recognized channels. There are markedly fewer inorganic anion transporters (5.1% — 18 total), including 6 primary carriers and 10 secondary carriers. In comparison, there are relatively few electron transport systems in Mxa. Table 5 Counts of Mxa transport proteins according to substrate type Substrate No. of proteins of indicated type acting on substrate type   Channels/Pores Primary carriers Secondary carriers Group translocators Transmembrane electron flow carriers Auxiliary proteins (Putative) Poorly characterized Total no. of systems I. Inorganic molecules                 A. Nonselective 3             3 B. Cations 6 36 38   1   3 84 C. Anions   6 10   2     18 D. Electrons   4     3     7 II. Carbon sources                 A. Sugars & polyols   4 2 2       8 B. Monocarboxylates               0 C. Di- & tricarboxylates     1         1 D. Organoanions (noncarboxylic)     2         2 E. Aromatic Compounds   4           4 III. Amino acids & their derivatives                 A. Amino acids & conjugates   6 14         20 B. Amines, amides, polyamines, & organocations 1             1 C.

Proc Natl Acad Sci U S A 2011,108(45):E1045–1051 PubMedCentralPub

Proc Natl Acad Sci U S A 2011,108(45):E1045–1051.PubMedCentralPubMed 69. Jack DL, Yang NM, Saier MH Jr: The drug/metabolite transporter superfamily. Eur J Biochem 2001,268(13):3620–3639.PubMed 70. Dalbey RE, Wang P, Kuhn A: Assembly of bacterial inner membrane proteins. Annu Rev Biochem 2011, 80:161–187.PubMed

71. Saller MJ, Fusetti F, Driessen AJ: Bacillus subtilis SpoIIIJ and YqjG function in membrane protein biogenesis. J Bacteriol 2009,191(21):6749–6757.PubMedCentralPubMed 72. Otani M, Kozuka S, Xu C, Umezawa C, Sano K, Inouye S: Protein W, a spore-specific protein in Myxococcus xanthus, formation of a large electron-dense particle in a spore. Mol Microbiol 1998,30(1):57–66.PubMed 73. Kuner JM, Kaiser D: Fruiting body morphogenesis in submerged cultures of Myxococcus xanthus. J Bacteriol Sepantronium solubility dmso 1982,151(1):458–461.PubMedCentralPubMed 74. Kim YM, Kim JH: Formation and dispersion of mycelial pellets of Streptomyces coelicolor A3(2). J Microbiol 2004,42(1):64–67.PubMed 75. Elizarov SM, Danilenko VN: Multiple

phosphorylation of membrane-associated calcium-dependent protein serine/threonine kinase in Streptomyces fradiae. FEMS Microbiol Lett 2001,202(1):135–138.PubMed 76. Padan E, Bibi E, Ito M, Krulwich TA: Alkaline pH homeostasis in bacteria: new insights. Biochim Biophys Acta 2005,1717(2):67–88.PubMedCentralPubMed 77. Yen MR, Tseng YH, Nguyen EH, Wu LF, Saier MH Jr: Sequence and phylogenetic analyses of the twin-arginine targeting buy ICG-001 (Tat) protein export system. Arch Microbiol 2002,177(6):441–450.PubMed 78. Palmer T, Berks BC: The twin-arginine translocation (Tat) protein export pathway. Nat Rev Microbiol 2012,10(7):483–496.PubMed 79. Hvorup RN, Winnen B, Chang AB, Jiang Y, Zhou XF, Saier MH Jr: The multidrug/oligosaccharidyl-lipid/polysaccharide (MOP) exporter superfamily. Eur J Biochem 2003,270(5):799–813.PubMed Fossariinae 80. Ruiz N: Bioinformatics identification of MurJ (MviN) as the peptidoglycan lipid II flippase in Escherichia coli. Proc Natl Acad Sci U S A 2008,105(40):15553–15557.PubMedCentralPubMed

81. Vasudevan P, McElligott J, Attkisson C, Betteken M, Popham DL: Homologues of the Bacillus subtilis SpoVB protein are involved in cell wall metabolism. J Bacteriol 2009,191(19):6012–6019.PubMedCentralPubMed 82. Fay A, Dworkin J: Bacillus subtilis homologs of MviN (MurJ), the putative Escherichia coli lipid II flippase, are not essential for growth. J Bacteriol 2009,191(19):6020–6028.PubMedCentralPubMed 83. Mohammadi T, van Dam V, Sijbrandi R, Vernet T, Zapun A, Bouhss A, Diepeveen-de Bruin M, Nguyen-Disteche M, de Kruijff B, Breukink E: Identification of FtsW as a transporter of lipid-linked cell wall precursors across the membrane. Embo J 2011,30(8):1425–1432.PubMedCentralPubMed 84.

In addition three of the four tryptophans, which are present in a

In addition three of the four tryptophans, which are present in all intimin subtypes [27], are also present in Ifp and invasin (Figure 1). Figure 1 Amino acid alignment of intimin, ifp and invasion. The C-terminal 280 residues of EPEC 2348/69 intimin (Int280) and the corresponding regions from Y. pseudotuberculosis IP32953 Ifp and invasin were aligned. Residues important in intimin function are shown: conserved cysteine residues are highlighted CRT0066101 mouse in light grey whilst tryptophan residues are highlighted in dark grey. Thermoregulated temporal expression of ifp and inv The expression of ifp (YPTB1572) and inv (YPTB1668) at 24°C, 28°C and 37°C, were monitored using lux-based promoter fusions

PI3K inhibitor 1572lux and 1668lux in Y. pseudotuberculosis IP32953,

with the resultant luminescence read in a Lucy1 combined photometer and luminometer (Figure 2). The expression was determined as relative light units/optical density (RLU/OD) therefore the growth phase could also be determined, based on these OD readings (Additional file 2). Inv was maximally expressed during log phase after 5 hours at 24°C and 28°C, but after only 2.5 hours at 37°C, suggesting that mammalian body temperature is important in the induction of inv and confirms the observation of Isberg et al. [38]. In contrast, ifp expression remains low at 24°C and 28°C throughout the time course, whereas at 37°C there was little expression in first 7.5 hours, after which expression increases to a peak at 13 hours (Figure 2). Figure 2 Temporal expression of ifp ( 1572lux ) and inv ( 1668lux ). Expression was determined by light emission from lux-reporter strains grown at (A) 24°C, (B) 28°C and Succinyl-CoA (C) 37°C. Three biological replicates are shown for each strain, with each biological replicate tested in triplicate. Ifp binds to localised foci on HEp-2 cells Invasin and intimin are able to bind directly to specific receptors on the surface of mammalian cells. We therefore investigated the ability of Ifp to bind directly to HEp-2 cells using a MBP tagged Ifp purified protein (MBP-Ifp). In addition, to determine if the terminal

cysteine was as important in Ifp functionality (as it is in invasin and intimin), a MBP-Ifp recombinant protein with the terminal cysteine mutated to a glycine (MBP-IfpC337G) was constructed and tested. Utilising flow cytometry, FACScan analysis showed a shift in the peak of fluorescence of HEp-2 cells which had been incubated with MBP-Ifp (Figure 3). This shift was not seen with cells incubated with MBP-IfpC337G or MBP alone, indicating not only that this is a specific binding of MBP-Ifp, but also that the terminal cysteine is important in the functional binding of Ifp to HEp-2 cells. However, MBP-Ifp only appears to bind to a subset of cells and to differing levels, as shown by the width of the shifted peak.

The histological changes in DEN-induced liver cancer in rats are

The histological changes in DEN-induced liver cancer in rats are similar to those seen in human HCC. We think the similar phenotype might be based on similar gene expression profiles. Affymetrix GeneChip Rat 230 2.0 arrays were used to analyze gene expression profiles of liver tissues from control and DEN-treated

rats during the process from cirrhosis to metastasis. This allowed us to obtain an almost complete picture of the early genetic alterations that are 4SC-202 directly or indirectly involved in the development of HCC. We supposed that the genes expression profiles deregulated during the process from liver cirrhosis to carcinoma and metastasis play key roles in the hepatocarcinogenesis. The data obtained from the gene expression profiles will allow us to acquire insights into the molecular mechanisms of hepatocarcinogenesis and identify specific genes (or gene products) that can be used for early

molecular diagnosis, risk analysis, prognosis prediction, and development of new therapies. Materials and methods Animals and treatments Male Wistar rats weighing 120–150 g at the beginning of the experiments were obtained from SLAC Laboratory Animal Co. Ltd. (Shanghai). The animals were PI3K inhibitor acclimatized to standard laboratory conditions (temperature 22–25°C, relative humidity 50–60%, and 12 hour photoperiods (lights on 07:00–19:00 h)) and were housed in stainless steel wire-mesh cages (five rats per cage). During the entire period of study, the rats were supplied with a semi-purified basal diet (Shanghai) and water ad lib. All experiments followed the Guide for the Care and Use of Laboratory Animals. Briefly, ninety Wistar rats were randomly divided into two groups: the control and DEN group (DEN, Sigma Chemical Co. St Louis, MO; CAS 56-23-5; purity > 98%). After one week on a basal diet, rats belonging to the DEN group underwent intragastric administration of 1% aqueous solution of DEN (70 mg/kg) once a week, consecutively for 14 weeks. Animals that belonged to the control group received distilled water. There were ten rats in the control group. Daily food and water intakes were noted

and the body weights of the animals from each group were recorded every second day. The rats were sacrificed Amino acid with 25% (g/ml) urethane anesthesia (6 ml/kg) by intraperitoneal injection and sacrificed at different time points. At the end of the 2nd, 4th and 6th week after DEN-treatment, 3, 3, and 4 rats were sacrificed respectively at these time periods. From the end of the 8th week until the end of the 20th week after DEN-treatment, ten rats were sacrificed respectively every two weeks. Meanwhile one age-matched control rat was sacrificed. All the age-matched rats from the control group and rats of treatment groups were sacrificed on the same day. Sample collection and histopathological analyses Animals were chosen sequentially for necropsy.

5 V, while for the point contacts in Figure 5c, the threshold vol

5 V, while for the point contacts in Figure 5c, the threshold voltage does not exceed 1 V. It is also noticed that there is a different response of the I-Vs in the two metal-dielectric-metal devices.

Figure 5 C -AFM measurements of a- TaN x . (a) Positive I-V curves (solid lines) of TaN x deposited on Au for four different points fitted by the space-charge-limited current (SCLC) model (dash lines). (b) Negative I-V curves (solid lines) of TaN x deposited on Au for the same points presented in (a) fitted by the SCLC selleck compound model (dash lines). (c) Positive I-V curves of TaN x deposited on Si for three different points. The conductive part of the I-Vs exhibits an CHIR-99021 almost parabolic to almost ohmic behavior (d) Negative I-V curves of TaN x deposited on Si for the points presented

in (b). In all I-Vs, the leakage current is quite high, displaying also a very noisy profile. In general, the total current flowing through a semiconductor can be written as I tot = I b + I s, where I b is the current from the bulk part of the film and I s includes the electronic conduction through the surface states and through the space charge layer beneath the surface. Taking into account the amorphous nature of the semiconducting film, the main conduction mechanism from the bulk is expected to be the Poole-Frenkel effect [43]. Usually in amorphous materials, the predominant

conduction mechanism is the Poole-Frenkel effect, i.e., the thermal emission of electrons from charged vacancies, attributed to impurities and defects that are present in large numbers inside the bulk of the amorphous matrix [43, 44]. In the present samples, charged nitrogen vacancies act like Coulombic traps that promote the injection of electrons from the Au or Ag bottom electrode as the electric field increases during forward bias direction and from Pt/Ir tip during the reverse bias direction. For Poole-Frenkel emission, the current density is given by [45]: (1) where C and β are material dependent constants, E is the induced electric field, q is the electron charge, T is the temperature, k is the Boltzmann HSP90 constant, and φ is the ionization potential in V. The constant C is related to charge carrier mobility and trap’s density, while β is related to the dielectric constant ε 0 ε r via (2) Other possible charge carrier transport mechanisms from the bulk of the film could be thermionic emission of charge carriers across the metal-dielectric interface or field emission by electron tunneling from the metal or charge traps to the quasi-conduction band of the amorphous semiconductor [46]. These mechanisms have also exponential like I-V behavior.

To assess for differences between outcomes in the intervention an

To assess for differences between outcomes in the intervention and control groups, multi-level hierarchical modelling using the General Estimating Equation (GEE) approach was used to account for clustering to estimate the treatment effect as an odds ratio and test for significance [33, 34]. First-order interaction terms (specifically: sex by intervention status) were evaluated. The 95% confidence intervals and p values were calculated using the sandwich estimator of variance.

The analysis was carried out using R: A Language and Environment for Statistical Computing version 2.10.1 [35, 36]. The GEE models were fit using the R package geepack selleck kinase inhibitor version 1.0-17. Results Study flow Of the 54 eligible hospitals, 36 agreed to participate and

were randomly assigned to intervention or control group (18 in each group). We obtained 801 records for fracture patients within 3 months of their admission to the ED; 139 were received 3 months after fracture. Of these, 443 were excluded: 298 were unable to reach, 51 had died or were in long-term care, 43 lived outside of the hospital catchment area, 21 refused, 18 had previously been screened by a fracture clinic coordinator and 12 had significant cognitive or hearing impairment, resulting in 358 enrolled subjects (Fig. 1). Fig. 1 Flow of patients through the trial Cluster size was comparable between the groups with ten (range, 3–16) Unoprostone learn more in the intervention and ten (range, 4–18) in the control hospitals. Of those randomized, 52 from the intervention hospitals and 39 from the control hospitals were lost to follow-up

leaving a total of 267 subjects with complete data for analysis. The primary analysis is a ‘complete case’ and includes only those whose outcome is known [37]. A secondary analysis was the strict intention to treat analysis in which all randomized subjects were included. Baseline characteristics The mean age of the study participants was 66.0 years in the intervention and 65.4 in the control group; about two thirds were female and married. Twenty-seven percent had a history of a previous fracture since the age of 40 years, 20% were current smokers and 23% had fallen in the previous 12 months. Thirty-one percent had a BMD test in the previous 12 months, 25% self-reported a diagnosis of osteoporosis and 19% were currently taking osteoporosis medications. The most common fracture type was wrist (34%), followed by ankle (16%), rib (12%), shoulder (12%) and hip (8%). There was no significant difference in demographic and clinical characteristics among patients in the intervention and control groups (Table 1).

The relative quantification was depicted as the fold-change in ex

The relative quantification was depicted as the fold-change in expression of each gene using the formula 2ΔΔCt, as previously described [33]. Each assay was performed in duplicate. Western blot analysis The antibodies to MRE11 were purchased from Santa Cruz Biotechnology (Sc-22,767), hTERT (ab-32,020) and POT1 (ab-124,784)

were purchased from Abcam, TRF2 (05-521) was purchased from Millipore, and the antibodies to Ku80 (2753S) and beta-Actin (4967S) were purchased from Cell Signaling Technology. Tumor extracts were homogenized SHP099 research buy and then lysed. The protein concentration was determined using the Bio-rad Dc Protein Assay Kit (Bio-rad). Equal amounts of proteins were subjected to sodium dodecyl sulfate 10% polyacrylamide gel electrophoresis (MiniProtean TGX, BioRad) and fractionated proteins were transferred to PVDF membranes (Transblot Turbo, BioRad). These membranes were blocked in TBS containing 5% nonfat milk, 0.05% Tween 20, and then probed with the appropriate antibody followed by incubation with a secondary IgG HRP-linked antibody (Cell Signaling Technology). The blots were then developed using an enhanced chemiluminescence detection system (Clarity Western ECL, BioRad). Immunocytochemistry Ki67 was assessed using Selleckchem Ro-3306 the anti-Ki67 MoAbs (clone MIB-1 Dako,

on BenchMark Ventana XT). CC1 treatment (1/50) was performed before ultraview revelation. Ki67 immunohistochemistry was quantified by a pathologist. The percentage of labeled nuclear area over the total neoplastic and the non-neoplastic nuclear area

Flavopiridol (Alvocidib) in the section was quantified from 2000 cells in areas of highest nuclear labeling. Statistical analysis Statistical analysis was performed using the 2-tailed Student’s t test or the Mann–Whitney U rank sum test. P < 0.05 was considered statistically significant in all analyses. All data analyses were performed using SPSS statistical software version 20. Results The main objective of this study was to determine whether differences exist in telomere deregulation between HBV-, HCV-, and alcohol-associated liver carcinogenesis. Liver carcinogenesis is a multistep process where clinical and histopathological features frequently permits the differentiation of the two main phases that include a cirrhotic stage followed by the development of overt HCC. Our collection of 80 liver samples was obtained from 40 patients with HCC. For each case 2 samples were analyzed that corresponded to tumoral and peritumoral tissue. The Table 1 shows that in 12 cases of HCC, peritumoral samples corresponded to histologically normal, non-cirrhotic liver tissue whereas in the 28 remaining cases, the peritumoral tissue was cirrhotic. We assumed that the development of cirrhosis from a histologically non-cirrhotic liver represents an early event during liver carcinogenesis, whereas the development of HCC from a cirrhotic liver reflects later carcinogenic events.

Bacteremic and nonbacteremic pneumococcal pneumonia

A pr

Bacteremic and nonbacteremic pneumococcal pneumonia.

A prospective study. Medicine. 2000;79(4):210–21.PubMedCrossRef 38. Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44(Suppl 2):S27–72.PubMedCrossRef 39. Broome CV, Facklam RR. Epidemiology of clinically significant isolates of Streptococcus pneumoniae in the United States. Rev Infect Dis. 1981;3(2):277–81.PubMedCrossRef 40. Potgieter PD, Hammond JM. The intensive care management, AZD6244 research buy mortality and prognostic indicators in severe community-acquired pneumococcal pneumonia. Intensive Care Med. 1996;22(12):1301–6.PubMedCrossRef 41. Tleyjeh IM, Tlaygeh HM, Hejal R, Montori VM, Baddour LM. The impact of penicillin resistance on short-term mortality in hospitalized adults with pneumococcal pneumonia: a systematic review and meta-analysis. Clin Infect Dis. 2006;42(6):788–97.PubMedCrossRef 42. Baddour LM, Yu VL, Klugman KP, Feldman C, Ortqvist A, Rello

J, et al. Combination antibiotic therapy lowers mortality among severely ill patients with pneumococcal bacteremia. Am J Respir Crit Care Med. 2004;170(4):440–4.PubMedCrossRef TGF-beta inhibitor 43. Aspa J, Rajas O, Rodriguez de Castro F, Huertas MC, Borderias L, Cabello FJ, et al. Impact of initial antibiotic choice on mortality from pneumococcal pneumonia. Eur Respir J. 2006;27(5):1010–9.PubMed 44. Kalin M, Ortqvist http://www.selleck.co.jp/products/Paclitaxel(Taxol).html A, Almela M, Aufwerber E, Dwyer R, Henriques B, et al. Prospective study of prognostic factors in community-acquired bacteremic pneumococcal disease in 5 countries. J Infect Dis. 2000;182(3):840–7.PubMedCrossRef 45. Sandvall B, Rueda AM, Musher DM. Long-term survival following pneumococcal pneumonia. Clin Infect Dis. 2013;56(8):1145–6.PubMedCrossRef

46. Hook EW 3rd, Horton CA, Schaberg DR. Failure of intensive care unit support to influence mortality from pneumococcal bacteremia. JAMA. 1983;249(8):1055–7.PubMedCrossRef 47. Ortqvist A, Grepe A, Julander I, Kalin M. Bacteremic pneumococcal pneumonia in Sweden: clinical course and outcome and comparison with non-bacteremic pneumococcal and mycoplasmal pneumonias. Scand J Infect Dis. 1988;20(2):163–71.PubMedCrossRef 48. Alanee SR, McGee L, Jackson D, Chiou CC, Feldman C, Morris AJ, et al. Association of serotypes of Streptococcus pneumoniae with disease severity and outcome in adults: an international study. Clin Infect Dis. 2007;45(1):46–51.PubMedCrossRef 49. Yu VL, Chiou CC, Feldman C, Ortqvist A, Rello J, Morris AJ, et al. An international prospective study of pneumococcal bacteremia: correlation with in vitro resistance, antibiotics administered, and clinical outcome. Clin Infect Dis. 2003;37(2):230–7.PubMedCrossRef 50. Vardakas KZ, Matthaiou DK, Falagas ME.

The nominal compression stress and strain are respectively determ

The nominal compression stress and strain are respectively determined by: (4) (5) where R particle is the initial radius of particle, P plate is the total reactive force of beads onto the plate, D is the displacement of the plate, and D 0 is the gap distance between the plate and particle prior to compression. Figure 4b presents the nominal compression stress–strain curves of the PE particles with different chain architectures. In general, highly nonlinear stress–strain behaviors Small molecule library are observed which resulted from the change in contact area during the simulation as well as the usual increase in hydrostatic

loading during compression, similar to experimental observations [19–21]. Four different regimes of compression behaviors can be identified from Figure 4b. In the first regime, it is observed that the slope of

the compression stress–strain curve has a sudden change at a strain around 0.06. This regime is primarily associated with the compression of the outer surface of Belnacasan the particle, which has a mass density that is lower than the inner bulk-level density and a depth of the interfacial thickness. As the applied deformation approaches a strain of 0.06, this lower density region becomes highly compressed and the overall compressive load starts transferring to the denser material under the surface. The second regime begins with the sudden increase in load due to this transfer of load to the denser subsurface. This behavior in this regime is similar to that observed in the initial phase of compression of micron-sized polymeric particles [19–21], in which the ratio of surface Fossariinae thickness to radius is very small. The third regime is associated with brief window strain softening, as indicated by the gray-shaded region in Figure 4b. This behavior is caused by an increase in molecular rearrangements that serve to temporarily relax the applied compressive load. In the fourth regime, significant

hardening occurs that is typical of uniaxial compression testing of polymers. This hardening is associated with the buildup of hydrostatic compressive forces within the particle. The effective compression moduli from the first, second, and fourth regimes were obtained by fitting the initial linear portions of the curves and are listed in Table 2. Comparison of these moduli for different chain architectures for each regime indicates that the stiffness of the network polymeric particle is consistently higher than that of the branched particle, which is consistently higher than that of the linear chain particle for all of the regimes. Therefore, the chain architecture plays a leading role on the compression behavior of PE nanoparticles. Figure 4 Compression stress and compression strain. (a) Schematic of the compression simulation of nanoscale PE particles. Beads are colored according to the molecular number. (b) Compressive stress–strain behaviors of PE nanoparticles with different molecular structures. Bold lines are the average of particle response.