Inte J Syst Proteases inhibitor Bacteriol 1989, 39:159–167.CrossRef 21. SGC-CBP30 molecular weight Grimont F, Grimont P: The genus Enterobacter. In The Prokaryotes. 3rd edition. Edited by: Dworkin M, Falkow S, Rosenberg E, Schleifer

K-H, Stackebrandt E. Singapore: Springer; 2006:197–214.CrossRef 22. Grimont F, Grimont P: The Proteobacteria. vol 2. In Bergey’s Manual of Systematic Bacteriology. 2nd edition. Edited by: Brenner D, Krieg N, Staley J, Garrity G. Singapore: Springer; 2005:587–850. 23. Hoffmann H, Stindl S, Ludwig W, Stumpf A, Mehlen A, Heesemann J, Monget D, Schleifer KH, Roggenkamp A: Reassignment of Enterobacter dissolvens to Enterobacter cloacae as E. cloacae subspecies dissolvens comb. nov. and emended description of Enterobacter asburiae and Enterobacter kobei . Syst Appl Microbiol 2005, 28:196–205.PubMedCrossRef 24. Hormaeche E, Edwards PR: Observations on the genus Aerobacter with a description

of two species. Int J Syst Evol Microbiol 1958, 8:111–116. 25. Bouvet OMM, Lenormand P, Grimont PAD: Taxonomic diversity of the D-glucose oxidation pathway in the Enterobacteriaceae . Int J Syst Evol Microbiol 1989, GSK2126458 39:61–67. 26. Wang GF, Xie GL, Zhu B, Huang JS, Liu B, Kawicha P, Benyon L, Duan YP: Identification and characterization of the Enterobacter complex causing mulberry ( Morus alba ) wilt disease in China. Eur J Plant Pathol 2009, 126:465–478.CrossRef 27. Kim KY, Hwangbo H, Park RD, Kim YW, Rim YS, Park KH, Kim TH, Suh JS: 2-Ketogluconic mafosfamide acid production and phosphate solubilization by Enterobacter intermedium . Curr Microbiol 2003, 47:87–92.PubMedCrossRef 28. Reinhold-Hurek B, Hurek T: Living inside

plants: bacterial endophytes. Curr Opin Plant Biol 2011, 14:435–43.PubMedCrossRef 29. Sessitsch A, Hardoim P, Döring J, Weilharter A, Krause A, Woyke T, Mitter B, Hauberg-Lotte L, Friedrich F, Rahalkar M, Hurek T, Sarkar A, Bodrossy L, Van Overbeek L, Brar D, Van Elsas JD, Reinhold-Hurek B: Functional characteristics of an endophyte community colonizing rice roots as revealed by metagenomic analysis. Mol Plant Microbe In 2012, 25:28–36.CrossRef 30. Stevens P, Van Elsas JD: Genetic and phenotypic diversity of Ralstonia solanacearum biovar 2 strains obtained from Dutch waterways. Antonie Van Leeuwenhoek 2010, 97:171–88.PubMedCrossRef 31. Pruesse E, Quast C, Knittel K, Fuchs BM, Ludwig W, Peplies J, Glöckner FO: SILVA: a comprehensive online resource for quality checked and aligned ribosomal RNA sequence data compatible with ARB. Nucleic Acids Res 2007, 35:7188–96.PubMedCrossRef 32. Tamura K, Peterson D, Peterson N, Stecher G, Nei M, Kumar S: MEGA5: molecular evolutionary genetics analysis using maximum likelihood, evolutionary distance, and maximum parsimony methods. Mol Biol Evol 2011, 28:2731–9.PubMedCrossRef 33. Wilson K: Preparation of genomic DNA from bacteria. In Current Protocols in Molecular Biology. Edited by: Ausubel F, Brent R, Kingston R, Moore D, Seidman J, Smith J, Struhl K.

High rate of surgical site infection in the present study may be attributed YH25448 to contamination of the laparotomy wound during the surgical procedure. Perforated peptic ulcer is a serious condition with an overall reported mortality of 5%-25%, rising to as high as 50%

with age [5–7, 9, 11, 44]. In this study mortality rate was high in patients who had age ≥ 40 years, delayed presentation (>24 hrs), shock at admission (systolic BP < 90 mmHg), HIV positivity, low CD4 count (< 200 cells/μl) and concomitant diseases. Also gastric ulcers were associated with an increased mortality risk. Boey's score, which is a score based on scoring factors as shock on admission, confounding medical illness, and prolonged perforation, has been found to be a useful tool in predicting outcome [11]. In this study, Boey score was a good predictor of both mortality and postoperative

complication and therefore should be used in our setting as a tool for predicting outcome in patients with perforated peptic ulcers. Since tests for detecting H. Pylori was not possible in our patients due to logistic problems, we did not take this into consideration in our discussion. However the use of the ‘triple regime’ produced TEW-7197 mw excellent results in 82.6% of our patients which is comparable to the results from recent studies [3. 4, 21, 22, 45] which have successfully used simple closure AZD6094 cost followed by eradication of H-Pylori as a treatment for perforated peptic ulcer. This is in contrast to the earlier studies [46, 47] which reported emergency definitive surgery as a means to prevent recurrence and re-operation rates. These findings are extremely important for developing countries like Tanzania where delay in presentation often prevents any attempt at definitive surgery. Before generalizing the results of our study several important issues need to be addressed. First, since all the subjects in the present study underwent pen repair, results from this study may not fully

represent those after laparoscopic repair. Second, we did not study the association of H. pylori with the postoperative outcomes because of lack of necessary facilities at the study center. Third, Suplatast tosilate data obtained retrospectively and failure to detect HIV infection during window period may have underestimated the prevalence of HIV infection. Fourth, since our duration of postoperative follow up was relatively short, we could not estimate the long term effect of Graham’s omental patch. Conclusion Perforation of peptic ulcer remains a frequent clinical problem in our environment predominantly affecting young males not known to suffer from PUD. Simple closure with omental patch followed by Helicobacter pylori eradication was effective with excellent results in majority of cases despite patients’ late presentation in our center.

lactis were included for comparison. The graph is of the data from one experiment. Characterization of murinized L. monocytogenes: competitive index assays Four inlA sequences conferring enhanced invasion into CT-26 cells

were selected to be re-created in the chromosome of L. monocytogenes EGD-e. The mutations constituted Idasanutlin manufacturer two single aa changes for EGD-e A (Asn259Tyr) and EGD-e B (Gln190Leu). While three aa changes were introduced into EGD-e C (T164A, K301I, Q303E) and EGD-e D (S173I, L185F, L188I). These mutations were chosen based on the frequency of isolation in L. lactis (EGD-e B and C), the ability to attribute the phenotype to an aa change (EGD-e A) and the isolation of mutations all confined within one LRR (EGD-e D). A fifth strain was also created based on the Lmo-InlAm mutation [18], except with

Listeria optimized codons for 192Asn and 369Ser, and was used as a positive control (EGD-e InlA m *). Sequencing LY2228820 datasheet confirmed the integrity of the newly introduced mutations, with equivalent levels of InlA expressed on the surface of the strains as compared PXD101 research buy to EGD-e (assessed by western blot – data not shown). InlAm strain (termed EGD-e InlA m *) was compared to the parental EGD-e strain for invasion into Caco-2 and CT-26 monolayers. No differences in invasion (Figure 7a) or adherence (data not shown) were observed to Caco-2 cells, while the invasion of EGD-e InlA m Resveratrol * was significantly higher than EGD-e into CT-26 cells. We then compared the virulence of EGD-e and EGD-e InlA m * by competitive index (CI) assays via the intravenous (i.v.) (Figure 7b) or intragastric (i.g.) (Figure 7c) route in Balb/c mice. For i.v. inoculated mice, no differences in the kinetics of infection were observed for either strain (Figure 7b). This confirms that the two amino acid changes in InlAm do not impact on the virulence of EGD-e InlA m * once

the gastrointestinal tract is bypassed. However, EGD-e InlA m * was significantly more virulent when infected by the i.g. route, with higher counts obtained from livers and spleens and a significantly higher CI value (p < 0.001) for both day two (Liver 28.9, Spleen 10.6) and day three (Liver 24.9, Spleen 7.7 – Figure 7c). Neither strain was recovered form the liver nor spleen at day one post infection. Subsequent competitive index experiments were conducted by the i.g. route comparing EGD-e InlA m * against the strains expressing the InlA mutations identified by the CT-26 cell screen (Figure 7d). Of the four recreated strains, only EGD-e A (N259Y) gave a higher CI than EGD-e in the liver (0.19 vs 0.05) whereas identical values (0.12) were obtained for the spleens. Further experimentation will be required to access the contribution of the N259Y mutation, and it would be intriguing to see if the recombination of this mutation into EGD-e InlA m * would further enhance murine pathogenicity.

Therefore, the highly connected nodes in these networks, the hubs, represented #buy NCT-501 randurls[1|1|,|CHEM1|]# genes

that were differentially expressed under many conditions or which had several functions in the cell. Our analysis was based on data extracted from three different strains of Salmonella, and we cannot rule out that details may differ between the three strains. However, the general scape of the networks should remain strain independent. Network analysis was based in the genome of S. Typhimurium LT2 strain, which was different from the strains used to evaluate the stress response and to carry out mutations. However, a highly similarity in the genome composition of S. Typhimurium strains has been previously reported [21, 22]. For instance, the magnitude of the reported difference between S. Typhimurium strains was in one case of two genes located in prophages [21] while in another study selleck chemicals the similarity was higher than 98% with the greatest difference attributable again to the distribution of prophages

[22]. Hubs are considered the strength of scale-free networks from random failures and their Achilles’ heel for directed attacks [16]. In order to investigate whether hubs were formed by essential genes in bacterial cellular networks, we carried out directed attacks by mutation of selected hubs in both Network 2 and Network 3. This showed that deletion of genes that formed hubs in these networks did not affect growth, stress adaptation or virulence. Despite the proven essentiality of hubs in other networks, hubs do not seem to be indispensable in cellular networks. This makes cellular networks more resistant to directed attacks addressing the weakest point of the scale free topology. This conclusion was based on analyses of four out of the five most connected genes in both types of network and a limited number of stresses, and we cannot rule out that mutation affects before adaptation to stresses that we have

not assessed. To aid the reader in evaluation of result, a short description of our results in the light of the current knowledge of the five most connected genes in both networks is included below. The wraB gene of S. Typhimurium encodes the WrbA protein eliciting 94% sequence similarity to the E. coli WrbA protein [23]. WrbA was first suggested to be involved in the binding of the tryptophan repressor to the operator [24] and recently identified as a novel flavoprotein [25] with NAD(P)H-dependent redox activity and able to reduce quinones. It has been designated as a NAD(P)H:quinone oxidoreductase (NQO) type IV which are associated with oxidative stress [26]. However, in the current investigation, a wraB single mutant was found not to show any changes in phenotype under any of the tested conditions, including when subjected to oxidative stress by H2O2.

This vector contains a kanamycin resistance gene (positive selection marker) that allows the selection of bacteria that would have integrated the plasmid into the chromosome. This vector was delivered to A. amazonense by means of conjugation (the carbon source utilized was maltose instead

of sucrose) and one colony resistant to kanamycin was obtained, suggesting that the integration of the plasmid was successfully accomplished. The sacB gene (negative marker selection) of the vector is lethal in the presence of sucrose; therefore, the merodiploid strain (containing both wild-type and mutant alleles) was unable to grow in M79 (containing 10 g/L of sucrose). Subsequently, expecting that a recombination event could replace the selleck chemicals llc wild-type allele, the merodiploid strain was cultured for many generations in M79 containing maltose HKI-272 in vivo instead of sucrose.

Finally, this culture was plated in M79 containing sucrose to eliminate the bacteria that did IWP-2 ic50 not accomplish the second recombination event. Seven sucrose-resistant/kanamycin-sensitive colonies were chosen for PCR evaluation of the substitution of the mutant allele for the wild-type gene. Four colonies presented a band of 121 bp, indicating that the wild-type glnK was successfully substituted, whereas three colonies presented the 361 bp band, corresponding to the wild-type allele (Figure 3B). Furthermore, an additional PCR with primers flanking the recombination sites was performed, and it also

demonstrated a reduction of the amplicon sizes originated from the glnK mutants in relation to the wild type strain (Figure 3C). This latter result demonstrates that recombination occurred in the target site. Figure 3 glnK gene mutagenesis. A – Schematic diagram depicting the mutagenesis procedure (modified from Clerico et al., 2007 [42]). The vector pKΔK (pK19MOBSACB derivative) harbors the flanking regions of the glnK gene (red). This suicide plasmid was delivered by conjugation to A. amazonense and integrated in the target site (orange) by homologous recombination, generating a merodiploid strain (containing both, wild-type and mutant alleles) that was selected by kanamycin since there is a resistance marker (white) present C59 in the vector. The black box represents the region deleted. Subsequently, the merodiploid strain was cultivated and the cells that underwent a second recombination event were selected by sucrose, since the sacB marker present in the vector is lethal in the presence of this substance. The kanamycin-sensitive/sucrose resistant colonies were evaluated by PCR. B – Identification of the mutant strains by PCR using primers that flank the deletion site. The primers glnK_NdeI_up and glnK_BamHI_do utilized in this procedure are represented by the small green arrows in Figure 3A. NC – negative control, WT – wild type, MER – merodiploid, numbers – strains tested.

LPS consists of three major components: lipid A, core polysaccharides and O-linked polysaccharides. Lipid A, with its fatty acid anchors [lauric, find more myristic and sometimes palmitic acid], is an endotoxin primarily responsible for TNFα-mediated septic shock. The addition of myristic

acid to the lipid A precursor Selleck AICAR is catalyzed by the enzyme MsbB [3]. It has been shown that msbB Salmonella serovar Typhimurium exhibits severe growth defects in LB and sensitivity to bile salts (MacConkey) and EGTA-containing media. However, compensatory suppressor mutants can be isolated that grow under these conditions. One of these suppressor phenotypes results from a mutation in somA, a gene of unknown function [4]. msbB Salmonella Typhimurium BAY 80-6946 datasheet strains have recently been developed as potential anti-cancer agents that possess impressive anti-tumor activity in mice [5]. In a phase I clinical study msbB Salmonella were shown to be safe in humans when administered i.v. However, bacteria were rapidly cleared from the peripheral blood of humans and targeting to human tumors was only observed in few patients at the highest dose levels of 3 × 108 CFU/m2 and 1 × 109/m2 [6]. Toso et al. [6] noted that YS1646 (suppressed msbB strain, see below) grew

best in air without added CO2. The potential to grow in acidic and CO2-rich environments is a hallmark of pathogenic bacteria, enhancing persistence within phagocytes and survival inside the host. Sensitivity to CO2 and low pH of msbB Salmonella strains might explain poor colonization of tumors, which often contain

high levels of CO2 and lactic acid [7, 8] due to the Warburg effect, also known as aerobic glycolysis, whereby glucose uptake is elevated while oxidative phosphorylation is reduced, even in the presence of oxygen. Our previous work on suppressors of msbB Salmonella raised the possibility that secondary mutations could suppress sensitivity to 5% CO2 and acidic conditions. Here we report that the growth of msbB Salmonella is highly inhibited (greater than 3-log reduction in plating efficiency) in a 5% CO2 atmosphere in LB media as well as under low pH conditions Megestrol Acetate when compared to wild-type Salmonella. Furthermore, several CO2 resistant clones were selected from an msbB Salmonella transposon library (Tn5). Three mutations were mapped and all were shown to contain the Tn5 marker in the zwf gene, which encodes the enzyme glucose-6-phosphate-dehydrogenase and is tightly linked to the msbB gene. Results CO2 sensitivity of msbB Salmonella CO2 sensitivity was first observed when YS1646, an msbB purI Suwwan deletion strain of Salmonella Typhimurium, was plated on blood or LB plates and incubated in a 5% CO2 incubator (Caroline Clairmont, personal communication; Toso et al., 2002).

05) and 6 min post exercise at 12 weeks (p < 0.01) and tended to be increased

0 post exercise at 8 and 12 weeks (p < 0.10) relative to the control week. Figure 4 Changes in brachial blood blow at weeks 1, 4, 8, 12 were compared to control week by a paired t -test, ‡ p  < 0.01, * p  < 0.05 and + p  < 0.10. Figure 5 Changes in Brachial Diameter at weeks 1, 4, 8, 12 were compared to control week by a paired t -test, ‡ p  < 0.01, * p  < 0.05 and + p  < 0.10. Discussion Wilson et al. recently suggested that oral ATP supplementation can significantly impact athletic performance, skeletal muscle hypertrophy and recovery; however, the study did not utilize methodologies to investigate the potential check details mechanism for the observed ergogenic effects [6]. One of the proposed mechanisms of action of oral ATP administration is an increase in blood flow, resulting in improved oxygen and nutrient delivery

to the muscle. Enhanced blood flow to an exercising skeletal muscle is expected to improve removal of metabolic waste products such as lactate and urea. Following exercise nutrient delivery and cell swelling play a vital role in the skeletal muscle adaptation response. Improvements in blood flow conceivably would allow for greater delivery of nutrients for skeletal muscle repair following a muscle damaging bout of training resulting in www.selleckchem.com/products/YM155.html increases in muscle hypertrophy previously seen with oral ATP administration. The main finding of this study was that orally Ilomastat administered ATP as a disodium salt indeed increases blood flow in exercising animals and humans, most prominently during the recovery period from exercise. Significant improvements could be measured at a daily dose of 400 mg ATP in as little Tolmetin as one

week in the human study. Though the exact mechanism of oral ATP absorption is currently not fully understood, animal studies have shown that the chronic oral administration of ATP resulted in measurable changes in muscle metabolism, peripheral blood flow, and blood oxygenation [10, 14] and human studies have resulted in significant improvements in body composition and performance [4, 6]. Studies on the oral availability of ATP showed that it is unlikely that oral ATP administration will directly increase intramuscular ATP stores as a single dose of orally administered ATP in humans did not increase ATP concentrations in blood [15]. The measurement of circulating free plasma ATP derived from oral ATP supplementation is very unlikely because exogenous free ATP is rapidly taken up by blood components or is rapidly metabolized. Kichenin et al. showed, in rats, that chronic oral administration of ATP increased portal vein ATP concentration and nucleoside uptake by erythrocytes, which resulted in an increase in ATP synthesis in the erythrocytes [10].

PubMedCrossRef 20. Berghoff KR, Franklin ME Jr: Laparoscopic-assisted rectal foreign body removal: report of a case. Dis Colon Rectum 2005, 48:1975–1977.PubMedCrossRef 21. Agnew J: Some anatomical and

physiological aspects of anal sexual practices. J Homosex 1985, 12:75–96.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ EPZ6438 contributions SYY: conception and design, or acquisition Selleckchem GSK2879552 of data, or analysis and interpretation of data, have given final approval of the version to be published. MK: conception and design, or acquisition of data, or analysis and interpretation of data. SA: revising it critically for important intellectual content; AC: revising it critically for important intellectual content; HTT: have made substantial contributions to conception and design. SH: have made substantial contributions to conception and design. All authors read and approved the final manuscript.”
“Introduction Ischemia-reperfusion (IR) injury

represents a fundamental common pathway of tissue damage in a wide variety of disease and surgical processes such as major trauma, acute mesenteric ischemia, septic and hypovolemic shock, abdominal aortic aneurism surgery, and cardiopulmonary bypass [1, 2]. Interruption of blood supply results in ischemic injury to all body systems and especially to high metabolically active tissues; the intestine is a prominent example Salubrinal of a sensitive tissue to IR injury which is associated with high morbidity and mortality [1]. Paradoxically, restoration of blood flow to the ischemic tissue augments cell injury by delivering toxic mediators induced in the ischemic tissue into the circulation thus affecting distant organs. This might lead to the GPX6 development of systemic inflammatory response syndrome, which can progress to multiple organ failure and death [2]. Among the toxic mediators produced in the IR injured tissue are acute-phase proteins, pro-inflammatory cytokines, oxygen free radicals, and components of the complement system [3]. Emergency surgery and trauma situations

may require abbreviated procedures during the initial phase of shock and organ ischemia. Definitive procedures including anastomosis to restore bowel continuity are undertaken 24 hours or more afterward. Two common examples of such situations are the strategy of damage control surgery in seriously injured patients, and acute mesenteric ischemia. In damage control laparotomy the goal in the emergency surgery is to stop bleeding and to control spillage from the intestine. In the second operation, which is done after the patient’s deranged physiology is corrected, bowel anastomosis may be created. In mesenteric ischemia gangrenous segments of the bowel are resected, while fluid resuscitation continues. Not infrequently, the patient condition does not allow performing primary anastomosis.

Maughan H, Redfield RJ: Extensive variation in natural competence in Haemophilus influenzae . Evolution 2009, 63:1852–1866.PubMedCrossRef 49. Mell JC, Shumilina S, Hall IM, Redfield E2 conjugating inhibitor RJ: Transformation of natural genetic variation into Haemophilus influenzae genomes. PLoS Pathog 2011, 7:e1002151.PubMedCentralPubMedCrossRef 50. Power

P, Bentley S, Parkhill J, Moxon E, Hood D: Investigations into genome diversity of Haemophilus influenzae using whole genome sequencing of clinical isolates and laboratory transformants. BMC Microbiol 2012, 12:273.PubMedCentralPubMedCrossRef 51. Okabe T, Yamazaki Y, Shiotani M, Suzuki T, Shiohara M, Kasuga E, OTX015 research buy Notake S, Yanagisawa H: An amino acid substitution in PBP-3 in Haemophilus influenzae associate with the invasion to bronchial epithelial cells. Microbiol Res 2010, 165:11–20.PubMedCrossRef 52. Murphy TF, Lesse AJ, Kirkham C, Zhong H, Sethi S, Munson RS: A clonal group of nontypeable Haemophilus influenzae with two IgA proteases is adapted to infection in chronic obstructive pulmonary disease. PLoS One 2011, 6:e25923.PubMedCentralPubMedCrossRef 53. LaCross NC, Marrs CF, Gilsdorf JR: Population structure in nontypeable Haemophilus influenzae . Infect Genet Evol 2013, 14:125–136.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions DS conceived and coordinated the study, performed susceptibility

testing, analysed and interpreted data and wrote the first draft; BEK, YT, AJ, LS and AS contributed to study design; ILA designed and

Farnesyltransferase undertook molecular analyses (except MLST); LS analysed the PFGE data, DAC and MS were responsible Vorinostat in vivo for acquisition of MLST data and AJ advised on bioinformatics. All authors participated in interpretation of results, critically revised the draft for intellectual content and approved the final article.”
“Background Bronchiectasis is a significant cause of chronic respiratory disease resulting in irreversible abnormally dilated bronchi associated with chronic inflammation, chronic cough and sputum production [1]. It can be caused by physical obstruction or post infectious damage, genetic defects (as observed in cystic fibrosis), abnormal host defence or autoimmune disease but in many cases bronchiectasis is idiopathic [2]. In this study we have focussed on the examination of a cohort of patients that presented with non-CF bronchiectasis (NCFBr). Chronic airway infection contributes to the underlying pathogenesis of the disease, with progressive lung damage resulting from recurrent bacterial infections and inflammatory responses [3]. The most commonly cultured pathogens associated with sputum of NCFBr are Haemophilus influenzae and Pseudomonas aeruginosa with many isolated strains showing significant antibiotic resistance [1, 4]. In prior studies, individuals that were culture-negative for bacterial pathogens showed the mildest disease, whereas, those with P.

The presence of the free ionic groups makes possible to bind metal ions via a simple aqueous ion exchange procedure and a LY2874455 clinical trial posterior chemical

reduction step with a reducing agent, leads to obtain the nanoparticles within the thin film. However, NVP-BGJ398 Su and co-workers have demonstrated the incorporation of AgNPs with the use of strong polyelectrolytes, such as poly(diallyldimethylammonium chloride) (PDDA) and poly(styrene sulfonate) (PSS), without any further adjustment of the pH [42]. Although the film thickness of the polymeric matrix can be perfectly controlled by the number of layers deposited onto the substrate, a better control over particles size and distribution in the films are not easy to achieve with the in situ chemical reduction and as a result, only yellow coloration is observed. Our hypothesis for obtaining the color is due to a greater degree control

over particles (shape and size distribution) in the films with a real need of maintaining the aggregation state. To overcome this situation, we propose a first stage of synthesis of multicolorAgNPs (violet, green and orange) in aqueous polymeric solution (PAA) with a well-defined shape and size. A second stage is based on the incorporation of these AgNPs into a polyelectrolyte multilayer thin film using the layer-by-layer (LbL) assembly. To our knowledge, this is the first time that a study about the color formation based on AgNPs is investigated in films preserving the original color of the solutions. Methods Materials Poly(allylamine Cisplatin hydrochloride) (PAH) (Mw 56,000), Poly(acrylic acid, sodium salt) 35 wt% solution in water (PAA) (Mw 15,000), silver nitrate (>99% titration)

and boranedimethylamine complex (DMAB) were purchased from Sigma-Aldrich and used without any further purification. Synthesis method of the PAA-capped AgNPs Multicolor silver nanoparticles have been prepared by adding freshly variable DMAB concentration (0.033, 0.33 and 3.33 mM) to vigorously stirred solution which contained Sinomenine constant PAA (25 mM) and AgNO3 concentrations (3.33 mM). This yields a molar ratio between the protective and loading agent ([PAA]/[AgNO3] ratio of 7.5:1. The final molar ratios between the reducing and loading agents ([DMAB]/[AgNO3] ratio) were 1:100, 1:10 and 1:1. The reduction of silver cations (Ag+) and all subsequent experiments were performed at room conditions and stored at room temperature. More details of this procedure can be found in the literature [33]. Fabrication of the multilayer film Aqueous solutions of PAH and PAA with a concentration of 25 mM with respect to the repetitive unit were prepared using ultrapure deionized water (18.2 MΩ · cm). The pH was adjusted to 7.5 by the addition of a few drops of NaOH or HCl.