PubMedCrossRef 35. Caughey GE: The effect on human tumour necrosis factor

α and interleukin 1 production of diets NU7026 mouse enriched in n-3 fatty acids from vegetable oil or fish oil. American Journal of Clinical Nutrition 1995, 63:116–122. 36. Hellsten Y, Frandsen U, Orthenblad N, Sjødin B, Richter EA: VX-661 in vivo Xanthine oxidase in human skeletal muscle following eccentric exercise: a role in inflammation. J Physiol 1997,498(Pt 1):239–48.PubMed 37. Steensberg A, Keller C, Starkie RL, Osada T, Febbraio MA, Pedersen BK: IL-6 and TNF-alpha expression in, and release from, contracting human skeletal muscle. Am J Physiol Endocrinol Metab 2002,283(6):E1272–8.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions DH, as post-graduate student, was responsible for recruiting the study participants, applying the study HKI-272 intervention, recording the data and writing the first draft of the manuscript. GLO, as his director of study developed the idea, trained DH in the laboratory skills, helped with the statistical analyses and refined the final version of the manuscript. Both authors read and approved the final manuscript.”
“Background Fluid loss during

strenuous, long duration exercise is commonplace and can result in thermal stress, impaired cognition and cardiovascular function, accelerated fatigue, and impaired exercise performance [1, 2]. Recommendations for fluid intake before, during, and following exercise are well described [3, 4] and are typically followed by most athletes seeking enhanced physical performance. Abiding by such recommendations appears

particularly important when exercising in hot and humid environmental conditions, where fluid loss may be high [5]. Although water is often suggested to many general fitness enthusiasts who may exercise for relatively short periods of time ( < 75 minutes), carbohydrate-electrolyte sport drinks are highly recommended and appear to be the beverage of choice for most serious athletes--aerobic athletes in particular [2]. This is partly fueled by scientific recommendations for the consumption of such beverages [6, 7], and partly by the widespread marketing campaigns of large sport Unoprostone nutrition and beverage companies. Regardless, carbohydrate-electrolyte beverages are widely consumed and represent a multi-billion dollar segment of the food and beverage industry [8]. Some individuals prefer natural alternatives to the manufactured sport drinks. For example, many sport drinks contain fructose and/or maltodextrin, artificial flavors and sweeteners, and added electrolytes (e.g., sodium, potassium). With more emphasis recently within the sport nutrition industry on “”natural”" beverages, some athletes and recreationally active fitness enthusiasts seek alternatives to the manufactured sport drink.

Figure 3 Metabolic activity of intracellular chlamydiae in infected monocytes and monocyte-derived DCs. Monocytes and monocyte-derived DCs were infected with C. trachomatis serovars Ba, D and L2 (MOI-3) and mock Emricasan control. 16S rRNA gene copy numbers was determined by isolating RNA at the indicated time points, followed by real-time PCR as described in materials and methods. 16S rRNA fold change was normalized to 18S rRNA and determined by ddCt method with mock sample

as reference gene. The mean of 3 independent experiments is shown and each experiment is pool selleck inhibitor of 2 donors. ***P < 0.001, **P < 0.01, *P < 0.05. In contrast 16S rRNA expression level was negligible in DCs for serovars Ba and D at 1 day p.i. and further declined with infection progression (Figure 3). Serovar L2 displayed highly significant expression of 16S rRNA at 1and 2 day p.i. Although the level declined on the 3 day p.i., the expression remained significant selleckchem (Figure 3).

To further characterize developmental state of chlamydial serovars within the infected monocytes and DCs, gene expression of euo, ompA and omcB were investigated. Each of these genes are known to be expressed at different developmental stages of chlamydiae (early, mid and late phase respectively), and have previously reported to be transcriptionally altered during chlamydial growth in human monocytes and DCs [40,42]. Figure 4 depicts the expression of the three genes in monocytes

and DCs respectively. Expression of the 3 genes within serovars Ba and D in both cell types was similar and stable, albeit at low levels in all the three time points that were investigated. Serovar L2 depicted a different pattern; early stage gene euo was significantly expressed 1 day p.i. compared to serovars Ba and D, gradually diminishing with time in both monocytes and DCs. The expression of mid-cycle gene ompA for serovar L2, although higher than the serovars Ba and D, was not statistically significant in infected monocytes. The expression for ompA within infected DCs peaked at 2 day p.i. significant to both serovars Ba and D. Expression of late stage gene omcB increased significantly 3 days p.i. for serovar L2 compared to serovars Ba and D in both monocytes and DCs. Figure 4 Quantification of euo , ompA and omcB gene expression in Methisazone chlamydiae infected monocytes and monocyte-derived DCs. Monocytes and monocyte-derived DCs were infected with C. trachomatis serovars Ba, D and L2 (MOI-3) and mock control. Copy numbers of euo, ompA and omcB genes were determined by isolating RNA at the indicated time points, followed by real-time PCR as described in materials and methods. Gene fold change was normalized to chlamydial 16S rRNA and determined by ddCt method with mock sample as reference gene. The mean of 3 independent experiments is shown and each experiment is pool of 2 donors. ***P < 0.001, **P < 0.01, *P < 0.05.

Deep-level emission has been reported to be caused by oxygen vacancies. Therefore, it indicated few oxygen vacancies existing in the ZnO films [14]. Figure 2 Room-temperature PL spectra of ZnO, InGaN, and GaN. The EL spectra of ZnO/InGaN/GaN heterojunction LED under various forward biases are shown in Figure 3a. The EL spectra were collected from the back face of the structure at room temperature. As shown in Figure 3a, with a forward bias of 10 V, a blue emission located at 430 nm was observed. Compared with the PL spectra,

it can CA4P mouse be easily identified that it originated from a recombination in the p-GaN layer. With bias increase, the blue emission peak shifted toward a short wavelength (blueshift). Note that mobility of electrons is faster than holes. Therefore, with low bias, electrons were injected from the n-ZnO side, through the InGaN layer, to the p-GaN

side, and little recombination occurred in the n-ZnO and InGaN layers. With bias increase, some holes can www.selleckchem.com/products/Trichostatin-A.html inject to the n-ZnO side. Hence, the intensity of emission from the ZnO increased, and as a result, the blue emission peak shifted toward a short wavelength. Additionally, with the bias increase, a peak centered at 600 nm was observed, as shown in Figure 3a. Compared with the PL spectra, the peak is not consistent this website with p-GaN, ZnO, and InGaN:Si. The peak under the bias of 40 V is thus fitted with two peaks by Gaussian fitting (Figure 3b). The positions of two peaks are 560 and 610 nm, respectively. The emission peak at 560 nm matches well with the PL spectrum of InGaN:Si. However, ID-8 the emission peak at 610 nm cannot

be found in the PL spectra. The PL emission of intrinsic GaN was at 360 nm, and GaN:Mg changes to 430 nm due to transmission from the conduction band and/or shallow donors to the Mg acceptor doping level. Hence, the peak centered at 610 nm might be from the Mg-doped InGaN layer [17]. Figure 3 EL spectra of ZnO/InGaN/GaN heterojunction LED under forward various biases (a) and multi-peak Gaussian fitting (b). The fitting are from experimental data at the range of 500 to 700 nm. Figure 4 illustrates the possibility of white light from the ZnO/InGaN/GaN heterostructured LEDs by the Commission International de l’Eclairage (CIE) x and y chromaticity diagram. Point D is the equality energy white point, and its CIE chromaticity coordinate is (0.33, 0.33). Because the points from 380 to 420 nm on CIE chromaticity diagram are very close, point A is used to represent the blue emission from p-GaN and ZnO. Points B and C represent emissions from InGaN:Si and InGaN:Mg, respectively. As shown in Figure 4, triangle ABC included the ‘white region’ defined by application standards. Therefore, theoretically speaking, the white light can be generated from the ZnO/InGaN/GaN LED with the appropriate emission intensity ratio of ZnO, InGaN:Si, InGaN:Mg, and p-GaN.

Therefore, a number of further studies with large sample sizes are needed to address this issue. Several limitations might be included in this study. Since most of the included studies have conducted on Asians and a few on Caucasians, the results must be interpreted with caution. Further studies concerning populations in other areas such as African and American are required to diminish the ethnic variation-produced biases. Additionally, MK5108 mouse a possible publication bias might have been introduced as only published studies written in English and Chinese as well as French that could be searched from Medline database were included. Notably, we did

not use the funnel plots and Egger’s linear regression test [33] for assessment of any possible publication biases because of the limited number of the included studies. Moreover, many factors may affect the results the funnel plots, leading to a misunderstanding of the publication biases [34, 35]. However, the fail-safe numbers failed to indicate evident publication biases. In this study, the

sample sizes of several studies in the meta-analyses are rather small, and, the pooled analyses were based upon a thousand cases and a thousand controls, this website which are under power to give a confirmed conclusion. Only two studies include three hundred cases and rest studies included less than one hundred cases. Authors need more cautions about their results. Furthermore, the controls of several studies were hospital-based normal individuals or patients with other Selleck TPCA-1 diseases. eltoprazine In addition, whether

the NPC and control groups were from the same socio-economic status or the same geographic area have not been clearly stated in some of the original papers. Hence, any selection biases might exist. Therefore, a number of further investigations regarding GSTM1 and GSTT1 polymorphisms and NPC risk are required. In conclusion, the data of the present meta-analyses indicate GSTM1 polymorphism as a risk factor for NPC and failed to show a significant association of GSTT1 polymorphism with NPC risk. Acknowledgements This work was supported by no funds. References 1. Lin CL, Lo WF, Lee TH, Ren Y, Hwang SL, Cheng YF, Chen CL, Chang YS, Lee SP, Rickinson AB, Tam PK: Immunization with Epstein-Barr Virus (EBV) peptide-pulsed dendritic cells induces functional CD8+ T-cell immunity and may lead to tumor regression in patients with EBV-positive nasopharyngeal carcinoma. Cancer Res 2002, 62: 6952–6958.PubMed 2. O’Neil JD, Owen TJ, Wood VH, Date KL, Valentine R, Chukwuma MB, Arrand JR, Dawson CW, Young LS: Epstein-Barr virus-encoded EBNA1 modulates the AP-1 transcription factor pathway in nasopharyngeal carcinoma cells and enhances angiogenesis in vitro. J Gen Virol 2008, 89: 2833–2842.

Transl Res. 2011; 158: 235−248. 40. Nakamura T, Kataoka K, Tokutomi Y, Nako H, Toyama K, Dong YF, et al. Novel mechanism of salt-induced glomerular injury: critical role of eNOS selleck kinase inhibitor and angiotensin II. J Hypertens. 2011;29:1528–35.PubMedCrossRef 41. Oudit GY, Herzenberg AM, Kassiri Z, Wong D, Reich H, Khokha R, et al. Loss of angiotensin-converting

enzyme-2 leads to the late development of angiotensin II-dependent glomerulosclerosis. Am J Pathol. 2006;168:1808–20.PubMedCrossRef 42. Reich HN, Oudit GY, Penninger JM, Scholey JW, Herzenberg AM. Decreased glomerular and tubular expression of ACE2 in patients with type 2 diabetes and kidney disease. Kidney Int. 2008;74:1610–6.PubMedCrossRef 43. Mizuiri S, Hemmi H, Arita M, Aoki T, Ohashi Y, Miyagi M, et al. Increased ACE and decreased ACE2 expression in kidneys from patients with IgA nephropathy. Nephron Clin Pract. 2011;117:c57–66.PubMedCrossRef 44. Velez JC, Ryan KJ, Harbeson CE, Bland AM, Budisavljevic MN, Arthur JM, et al. Angiotensin I is largely converted to angiotensin (1–7) and

angiotensin (2–10) by isolated rat glomeruli. Hypertension. 2009;53:790–7.PubMedCrossRef 45. Velez JC, Bland AM, Arthur JM, Raymond JR, Janech MG. Characterization of renin-angiotensin system enzyme activities in cultured mouse podocytes. Am J Physiol Ren Physiol. 2007;293:F398–407.CrossRef 46. Velez JC, Janech Nintedanib molecular weight MG, Arthur JM, Raymond JR. Cultured human glomerular endothelial cells display ACE-mediated angiotensin-II-generating capacity and limited

angiotensin-II-degrading activity. Am OICR-9429 molecular weight Soc Nephrol Annual Meeting; 2010 (in abstract). 47. Singh R, Singh AK, Alavi N, Leehey DJ. Mechanism of increased angiotensin II levels in glomerular mesangial cells cultured in high glucose. J Am Soc Nephrol. 2003;14:873–80.PubMedCrossRef 48. Cristovam PC, Arnoni CP, de Andrade MC, Casarini DE, Pereira LG, Schor N, et al. ACE-dependent and chymase-dependent angiotensin II generation in normal and glucose-stimulated human mesangial cells. Exp Biol Med. 2008;233:1035–43.CrossRef 49. Aragão DS, Cunha TS, Arita DY, Andrade MC, Fernandes AB, Watanabe IK, et al. Purification and characterization of angiotensin converting enzyme 2 (ACE2) from murine model of mesangial cell in culture. Int J Biol Macromol. 2011;49:79–84.PubMedCrossRef”
“A 56-year-old diabetic woman with 3-day history of urinary tract infection taking oral antibiotics presented with a sudden consciousness disturbance. On examination, a febrile (38.8°C) patient with a blood pressure of 83/48 mmHg and a heart rate of 120/min was seen. Laboratory studies revealed a leukocyte count of 11.0 × 109/l with band neutrophils of 22%. Urinalysis showed pyuria with 40–50 see more leukocytes per low-power field. Escherichia coli were found in both blood and urine cultures.

In many bacterial pathogens, cell envelope stress responses play a multifaceted role. They provide protection against damage caused by components of the immune system, such as complement and antimicrobial peptides that target the cell envelope [3–5]. They regulate the expression of chaperones required

for proper assembly of cell envelope-associated structures, including outer membrane porins, pili, and fimbrae [3, 6, 7]. In addition, cell envelope stress responses can sense the environment around the bacterium and regulate the expression of virulence factors in this website response to specific cues, ensuring that these factors are expressed at the proper time and location in the host [2, 8]. Despite their importance, no cell envelope stress responses have yet been identified or implicated in pathogenesis in Bordetella species. Bordetella bronchiseptica is a respiratory pathogen that is closely related to Bordetella pertussis S63845 mouse and Bordetella parapertussis, the

causative agents of whooping find more cough in humans [9, 10]. B. bronchiseptica causes a range of diseases in various mammals that can be chronic, difficult to completely eradicate, and of variable virulence [11–13]. It is the etiological agent of atrophic rhinitis in swine, kennel cough in dogs, and snuffles in rabbits [12, 13]. Documented human infections, generally traced to an animal source, have been observed in immunocompromised individuals, and can be serious, systemic infections [11, 14]. The B. bronchiseptica, B. pertussis and B. parapertussis genomes encode a large number of putative transcription factors relative to their overall genome size [15], suggesting that these pathogens have the capacity to extensively regulate gene expression in response to environmental and physiological changes. Despite this finding, only a few Bordetella transcription factors have been studied in any detail [16–20]. Among the predicted transcription factors is an ortholog of the cell envelope stress response sigma

factor, σE, of E. coli. In bacteria, sigma Pembrolizumab in vivo factors are the subunits of bacterial RNA polymerases required for specific promoter recognition and transcription initiation [21]. Alternative sigma factors, like σE, are activated in response to specific stresses and rapidly reprogram gene expression by replacing the housekeeping sigma factor and directing RNA polymerase to the genes in their regulons [21, 22]. σE belongs to the RpoE-like group of extracytoplasmic function (ECF) sigma factors that have been increasingly implicated as key factors contributing to both bacterial stress responses and virulence [23, 24]. These sigma factors are widely distributed across bacterial phyla. Where studied, they direct a diverse set of stress responses primarily targeted to the cell envelope [2, 8, 24, 25]. In E.

Positive values show phenotypes learn more gained in rpoS mutants while negative values show phenotypes lost because of rpoS mutations. In total, rpoS mutants grew better on 92 nitrogen sources tested, and the top 10 are listed. Enhanced growth of Suc++ (rpoS + and rpoS -) mutants is not limited to the TCA cycle intermediates To extend the phenotype screening results to pathogenic E. coli, we tested the growth of EDL933 and derivative rpoS and Suc++ (rpoS + and rpoS -) mutants on selected carbon sources (20 mM each) that best supported differential respiration of rpoS mutants relative to wild type (Transmembrane Transproters inhibitor Figure 4). Glucose and succinate were also tested as controls for comparison.

As expected, compared with wild type, the rpoS and Suc++ mutants grew similarly on glucose but much better on succinate. Among the Biolog compounds tested, MM-102 the rpoS and Suc++ mutants, including the Suc++(rpoS +) mutants, grew better than wild type on D-glucuronic acid or glutamine as the sole carbon source. However, none of these strains could grow on threonine or proline as the sole carbon source, which is likely due to differences in strain background and experimental conditions. The enhanced growth of mutants on D-glucuronic acid and glutamine confirmed that mutations selected on succinate have pleiotropic effects on utilization of other nutrient sources.

Figure 4 Growth of EDL933 and derivative mutants on different carbon sources. “”ND”": not detected. Cells were grown in LB media to OD600 0.6, washed and inoculated to fresh media to a starting OD600of 0.05. Cultures were then grown at 37°C with vigorous shaking (200 rpm) and sampled every hour for 10 hours to monitor growth. D-glucuronic acid, threonine, glutamine or proline were added to M9 minimal media as the sole carbon source to a final concentration of 20 mM.

Discussion Understanding how pathogens adapt and mutate in response to growth environments is critical in deciphering many of the unknowns regarding pathogenesis, such as the emergence of new pathogens, the increased resistance to antibiotics, and the long-term persistence in host environment. In this study, we report that a metabolic selection mechanism for loss of RpoS, a central stress Thiamet G and adaptation regulator, in representative verocytotoxin-producing E. coli strains, may be responsible for the occurrence of rpoS mutations among pathogenic E. coli isolates. In surveying the rpoS gene among E. coli isolates, we found many mutations in rpoS, some of which result in loss of RpoS function. Among the VTEC strains tested, most grow poorly on succinate (like laboratory K12 strains) but some strains grow well. Those that grow poorly all have intact rpoS. In contrast, strains that grow well on succinate can be distinguished into two groups, one with intact rpoS and the other with truncated rpoS.

as other organisms also produce yellow-colored colonies on TSA. In addition, it was found that not all Cronobacter spp. produces yellow color on TSA [2]. In a previous study, Farmer et al., [19] grouped 57 strains of E. sakazakii into 15 biogroups which later, Iversen et al., [40] expanded by using cluster analysis (based

on partial 16S rRNA sequence analysis) of 189 strains to include a 16th biogroup. This was followed by two proposals by Iversen et al. [41, 42] showing that this organism comprised of six related groups of strains that could be separated on the basis of DNA-DNA hybridization relatedness and phenotypic traits, into 5 novel selleckchem species and 1 novel genomospecies within a new genus named Cronobacter. These studies gave a clear indication of the genetic and phenotypic heterogeneity among these organisms. Therefore, it is important that the presence and the identity of Cronobacter spp. be confirmed by more than one method. Biochemical, chromogenic and molecular techniques such as PCR that amplify specific Cronobacter spp. genes and 16S rRNA sequencing analysis should be among the methods used for this purpose. The aims of this study therefore were to analyze a wide range of foods including infant foods, milk powder, herbs, and environmental samples in an attempt to find the reservoir for this pathogen CBL0137 ic50 and to compare the biochemical, cultural and molecular

methods for the proper identification and confirmation of Cronobacter spp. Methods Samples collection A total of 222 samples of food, infant formula, infant foods, herbs and spices originating from 14 different Navitoclax manufacturer countries were purchased from local markets. In addition, 11 environmental samples (vacuum dust and soil) were collected and tested for

the presence of Cronobacter spp. Isolation of Cronobacter spp It is noteworthy to mention that in this study two methods of Cronobacter spp. isolation were used. The FDA method [43] was used at the beginning of the project for the isolation of Cronobacter spp. from the food and herbal samples. However, during the project, a new modified method for the isolation of Cronobacter spp. was developed [2]. Thus, the new method was adopted for the isolation of Cronobacter spp. from infant formula and milk powder samples. Isolation of Cronobacter spp. from infant formula, Silibinin milk powder and infant foods A total of 76 samples (40 infant formulas and solid infant foods, 29 milk powder and 7 dairy non-milk foods) were tested for the presence of Cronobacter spp. using the method described by Iversen and Forsythe, [2]. Briefly, 100 g of infant food, milk powder or infant formula were added to 900 ml of peptone water and warmed up for 25 min at 45°C. Ten milliliters were then incubated in E. sakazakii enrichment broth (ESE) for 24 h at 37°C. From each enriched sample, 0.1 ml and 1 ml were streaked or spread onto Druggan Forsythe Iversen (DFI, Oxoid, UK,) agar and incubated for 24 h at 37°C.

The decomposition of H2O2 was measured by monitoring the decrease in absorbance at 240 nm using a microplate reader (Paradigm, Beckman Coulter). Each strain was run in five replicates.

The initial linear portion of the curve was used to calculate the Δ240 nm. A molar extinction coefficient of H2O2 at 240 nm of 43.6 M-1 cm-1 was used to calculated the concentration of H2O2 using the Beer-Lambert law, A = εcl. One unit of catalase was defined as the amount that decomposes 1 μmol of H2O2 per minute per OD600 at 25°C. Analysis of gene expression Bacteria were collected from cultures after 18 h of incubation and mixed with 50% (v/v) RNAlater (Qiagen, Hilden, Germany) and when needed, placed in -20°C, to stabilize the RNA until extraction could be performed. RNA was extracted

using Trizol Selleck PCI-34051 (Invitrogen) according to the manufacturer’s protocol. cDNA was synthesized from this RNA and quantitative buy Sapanisertib real-time PCR (RT-PCR) was used to analyze the cDNA samples. In order to remove contaminating DNA, the RNA samples were DNase-treated (DNA-free kit, Ambion, Inc, Austin, TX, USA) in accordance with the protocol supplied by the manufacturer. The RNA was quantified by Nanodrop (Thermo Fisher Scientific, Wilmington, DE, USA). cDNA was synthesized from 1 μg of the extracted selleck products RNA using iScript cDNA synthesis kit (Bio-Rad, Hemel, Hampstead, UK) according to the protocol provided by the manufacturer. To control for contaminating DNA in the RNA preparation, a control was prepared by substituting the enzyme from the cDNA synthesis for nuclease-free H2O (Ambion) (control 1). In order to degrade any remaining RNA, the cDNA

was treated with 2.0 μl of 2.5 M NaOH at 42°C for 10 minutes after which the pH was adjusted by the addition of 5 μl of 1 M HCl. The samples check details were thereafter diluted and stored at -20°C. RT-PCR was performed in the ABI Prism 7900HT Sequence Detection System (Applied Biosystems, Foster City, CA, USA) using the Power SYBR green PCR Master Mix (Applied Biosystems) as recommended by the manufacturer. Each reaction contained 12.5 μl of the SYBR green mix, 400 nM of forward and reverse primers, 5 μl of a cDNA and the total volume was adjusted with nuclease free water to 25 μl. Forward and reverse primers were obtained from Invitrogen and their sequences have been previously published [20, 23] with the exception of the pairs used to measure mglA, feoB and katG. The sequences for mglA were the following: FTT1275-F, 5′-TTG CAG TGT ATA GGC TTA GTG TGA-3′ and FTT1275-R, 5′-ATA TTC TTG CAT TAG CTC GCT GT-3′, for feoB: FTT0249-F, 5′-TCA CAA GAA ATC ACA GCT AGT CAA-3′ and FTT0249-R, 5′-CTA CAA TTT CAG CGA CAG CAT TAT-3′ and for katG the following: FTT0721c-F, 5′-TTC AAG TTT AGC TGG TTC ATT CAT-3′and FTT0721c-R, 5′-GCT TGG GAT TCA GCT TCT ACT TAT-3′. The reactions were performed in MicroAmp 96-well plates (Applied Biosystems).

Dislocation cores are represented by thin tubes, in which Shockley partial dislocation with 1/6 <112 > Burgers vector and perfect dislocation with 1/2 <110 > Burgers vector are colored gray and red, respectively. It is seen from Figure 4b that the dislocation loop learn more consists of four

partial dislocations and one perfect dislocation. In addition, there is one vacancy formed beneath the probe. Upon further penetration, the other buy Pexidartinib three 111 slip planes are activated sequentially, and Figure 4c shows that the defect zone beneath the probe expands greatly. The glide of dislocations on adjacent slip planes leads to the formation of stair-rod dislocations with 1/6 <110 > Burgers vector highlighted by the arrows in Figure 4d. Figure 4e,f presents dislocation network after the completion of scratching and penetration, respectively. It is seen from Figure 4e that there is less dislocations but more

vacancies in the wake of the probe than that in the vicinity of the probe due to the plastic recovery. In addition to the stair-rod dislocations, there are glissile prismatic dislocation loops formed by dislocation reaction and cross-slip events. In particular, the prismatic dislocation half-loops in front of the probe glide parallels to the free surface to transport the materials displaced by the probe without the formation of surface steps [24]. Although small part of the dislocations beneath the probe annihilates at the free surface during the retraction,

Figure 4f shows that the defect structures are stable. Figure check details 4 Close inspections of defect structures in friction with a probe radius of 8 nm. The scratching depth is 0.82 nm. (a,c) Bottom views of defect structures at penetration depths of 0.72 and 0.82 nm, respectively. Atoms are colored according to their BAD values and FCC atoms are not shown. (b,d) Dislocation networks shown in (a) and (c), respectively. (e,f) Dislocation networks after the completion of scratching and retraction, respectively. Effect of probe radius on minimum wear depth To investigate the influence of probe radius on the minimum wear depth, friction simulations acetylcholine with another three probe radiuses of 6, 10, and 12 nm are conducted, in addition to the probe radius of 8 nm. For each probe radius, the penetration stage stops at a penetration depth that is 0.1 nm deeper than the critical penetration depth at which the phenomenon of force drop occurs. Figure 5a,b plots the contact pressure-penetration depth curves and the friction coefficient-scratching length curves during the penetration and scratching stages with the four probe radiuses, respectively. The contact pressure is defined as the ratio of the penetration force to the contact area. A detailed description about the calculation of the contact area during spherical penetration can be found elsewhere [28].