ProteinLynx software (Version 2.2.5), provided by the manufacturers, was used to analyze raw MS and MS/MS spectra and to Dibutyryl-cAMP ic50 generate a peak list which was introduced in the in-house Mascot MS/MS ion search software (Version 2.2, Matrix Science, Boston, MA) for protein identification.

NCBI was used as sequence database. Search parameters were as follows: LY2874455 molecular weight fixed modifications carbamidomethyl (C), variable modifications pyro-Glu (N-term Q) and oxidation (M), peptide tolerance 30 ppm, MS/MS tolerance 0.3 Da, charge state +2 and +3, enzyme trypsin, allowing up to 1 missed cleavage. Data analysis MS data were subjected to gene ontology analysis with Blast2GO, using default parameters [57]. Identified proteins were divided into classes for functional and localization analysis; data produced by the software were used for generation of graphs by Microsoft Excel. Acknowledgements We thank Prof. Christine Citti for kindly providing the type strain PG2T, Dr. Mario Ferrer-Navarro for his helpful suggestions during optimization of the NVP-BGJ398 clinical trial protein fractionation approach, Dr. Vittorio Tedde and Dr. Alessandro Tanca for assistance during electrophoresis and MALDI-MS identification, and Dr. Stefania Ghisaura from Biosistema Scarl for the DIGE experiments. This work was supported by funding

from the Grant “”Ricerca Sanitaria Finalizzata, Anno 2007, UPB S02.04.010, Cap SC02.1106″”, and Misura P5 Biodiversità animale (Regione Sardegna). Electronic supplementary material Additional file 1: 2-D PAGE map of liposoluble proteins from M. agalactiae PG2 T illustrating the protein identifications obtained by MS on the 3-10NL pI Interval. (DOC 175 KB) Additional file 2: 2-D PAGE map of liposoluble proteins from M. agalactiae PG2 T illustrating

the protein identifications obtained by MS on the 7-11 pI Interval. (DOC 166 KB) Additional file 3: 2-D PAGE map of liposoluble proteins from M. agalactiae PG2 T illustrating the protein identifications obtained by MS on the 4-7 pI Interval. (DOC 94 KB) Additional file 4: Table listing all protein identifications obtained from 2-D PAGE maps. The proteins listed in this table were identified from 2-D PAGE maps of the M. agalactiae PG2T Triton X-114 Epothilone B (EPO906, Patupilone) fraction. Maps are represented in Additional files 1 (pH 3-10NL), 2 (pH 7-11) and 3 (pH 4-7). (DOC 568 KB) Additional file 5: Protein profile of liposoluble proteins before and after precipitation. Right: approach used for GeLC-MS/MS characterization. The bars indicate the regions cut from the PAGE gel and subjected to mass spectrometry characterization. Protein identifications are reported in additional file 6, from top to bottom. (DOC 96 KB) Additional file 6: Table listing all protein identifications obtained by GeLC-MS/MS of the M. agalactiae PG2 T Triton X-114 liposoluble fraction. The protein profile used and the number of slices are reported in Additional file 5.

With as little as 24 hours of gross contamination, inflammatory changes develop and may not only limit surgical

options but also predispose to the development of further complications [31]. The treatment options for an extrahepatic biliary leak have broadened. Until recently, such injuries usually mandated surgical repair utilizing debridement and closure with or without T-tube; patch closure using gallbladder, cystic duct, vein, serosa or jejunum; biliary enteric anastomosis using duodenum or jejunum; or ligation and drainage with plans for subsequent enteric diversion [32]. When the only relative indication for surgery is the bile leak, nonoperative management see more is possible [33]. In our case, during the last intervention, because of a biliary peritonitis and inflammatory changes due to the late diagnosis, the dissection of CBD and the direct approach to the biliary leak was considered dangerous and not indicated;

only the achievement of an external biliary fistula, well drained, was possible; therefore, a T-tube was placed in Selleckchem Blasticidin S the choledochus through the residual cystic duct stump, and not through the biliary leakage who was at the opposite and inaccessible aspect of the common bile duct. Also an abdominal drain was placed into the subhepatic region (Figure 2). This allowed to achieve a well drained external fistula, and consequently to dry up the biliary leak one month later. Our patient returned to full activity, had normal serum hepatic enzyme levels and no sequelae from her injury. Figure 2 Surgical management of the biliary leakage. An abdominal drain is placed into the porta hepatis area. A T-tube is placed in the choledochus through the residual cystic duct stump. Biliary leakage, on the left posterolateral Adenosine triphosphate aspect of the common bile duct, 1 cm below the biliary confluence, is highlighted in

yellow. Conclusions We present a case of an isolated extrahepatic bile duct rupture in blunt abdominal trauma. A literature review was conducted to detect all similar cases. Many few cases were found. Common bile duct injury is often discovered immediately during laparotomy. The diagnosis of a bile duct injury is often difficult in the multiply injured patient. The JAK inhibitor combination of suboptimal imaging modalities, the presence of confounding injuries, and the rare incidence of blunt traumatic CBD injuries contribute to the diagnostic challenge of these problems. Late recognition and inappropriate management of these injuries result in severe, often fatal consequences. The approach to the management of these patients depends primarily on the patient’s hemodynamic status. The principles of operative management in the unstable patient follow the guidelines of damage control laparotomy. The treatment options for an extrahepatic biliary leak have broadened.

Wang and Welch [4] showed that 24 of 50 patients were clinically asymptomatic in their case series of adolescents and adults with malrotation. Adults with a rotational abnormality of the gut usually present differently to paediatric patients. Two distinct patterns of adult presentations have GS-4997 research buy been reported in the literature: acute and chronic [5, 7, 9]. Chronic presentation is more common in adults. This is characterised by intermittent crampy abdominal pain, bloating, nausea and vomiting

over several months or years. The symptoms may be highly nonspecific. However, the range of clinical presentations, underlines the need for a high index of suspicion of midgut malrotation, when investigating the cause of intermittent and varying abdominal symptomatology in a healthy young adult [5, 7]. Dietz et al [5] studied a series of 10 adults with bowel obstruction caused by intestinal malrotation. They reported that 5 adults presented with chronic features and that the duration of symptoms

extended to 30 years. Fu et al [7] reported that 6 of 12 patients in their series presented with chronic intermittent abdominal symptoms. Diagnostic delays are common in this group of patients because of the nonspecific nature of the presentations. The pathophysiology of these chronic symptoms may relate to the compression effect of Ladd’s bands this website running from the caecum and ascending colon to the right abdominal wall [5, 10]. The other group of symptomatic HAS1 adults typically present with symptoms of acute bowel obstruction and these patients may or may not report a previous history of abdominal symptoms, CHIR-99021 cost as with our patient. These patients may on occasion, have symptoms and signs of an impending abdominal catastrophe. Moldrem et al

[9] reported that 48.5% of their thirty-three patients presented with an acute abdomen. Acute presentation may be due to volvulus of the midgut or ileocaecum, reported as the most common cause of bowel obstruction in adults with gut malrotation. Other causes of acute presentation may be related to internal herniation caused by Ladd’s bands. There is also a subgroup of acutely presenting adult patients with malrotation. They are identified when affected by other common abdominal diseases. Their unusual intestinal anatomy results in atypical signs and symptoms. These patients may present with localised peritonitis in the right upper quadrant or on the left side of the abdomen if their appendix becomes inflamed. The atypical presentations may lead to confusion, as one common abdominal pathology may mimics another, leading to incorrect diagnosis of conditions such as acute appendicitis, cholecystitis, pancreatitis, perforated peptic ulcer disease and left colonic diverticulitis. Several authors have reported observing atypical presentations of this nature before discovering gut malrotation with abnormal location of the caecum and appendix at surgery [5, 7].

Because the temperature gradient (corresponding to the temperature difference driving force) is small and the temperature is high in the lower left corner, the density of water in the lower left corner is thus low. For a high Rayleigh number (Ra = 1 × 105), the temperature gradient and the corresponding driving force become larger, then the lower-density water, including

that in the lower left corner, rises to the top CB-839 right corner. The denser water is cooled by the top wall and flows downward to the lower right corner, and the area where the denser water in the lower right corner becomes larger. Figure 6 Density KPT-330 supplier distribution of water phase at Ra = 1 × 10 3 (a) φ = 0.01 (b) φ = 0.03 (c) φ = 0.05. Figure 7 Density distribution of water phase at Ra = 1 × 10 5 (a) φ = 0.01 (b) φ = 0.03 (c) φ = 0.05. Figures 8 and 9 respectively present the nanoparticle distribution of nanofluid with volume fractions at Ra = 1 × 103 and Ra = 1 × 105. For a low Rayleigh number (Ra = 1 × 103), the driving force along the left wall is upward, and many nanoparticles are driven to the top right corner, which contributes to the high nanoparticle volume fraction in the top right corner. However, the temperature gradient

in the lower left corner is small and causes a correspondingly small temperature difference driving force. Thus, many nanoparticles are left in the lower left corner, which contributes to the high nanoparticle volume fraction in the lower left corner. There is a large temperature gradient in the lower right corner, and the large driving force displaces the nanoparticles off the lower right corner, which QNZ purchase contributes to the low nanoparticle volume fraction in the lower right corner. For a high Rayleigh number (Ra = 1 × 105), the convection heat transfer is enhanced and the velocity of the nanofluid becomes larger, and the temperature gradient and the corresponding driving force become bigger. Thus, many nanoparticles from the bottom are driven to the top by the driving force, which contributes to the low nanoparticle volume fraction enough at the bottom and a high nanoparticle

volume fraction at the top. In addition, we can see that the nanoparticle volume fraction distribution is opposite to that of the water-phase density distribution. From Table 4, we can see that the temperature difference driving force is the biggest one, and the changes of the water-phase density and the inhomogeneous nanoparticle distribution are mainly due to the driving force. Through the above analysis, it is found that the nanoparticles migrate to locations where the water density is small, and thus, the conclusion that the nanoparticle volume fraction distribution is opposite to that of the water-phase density distribution is obtained. Figure 8 Nanoparticle volume fraction distribution at Ra = 1 × 10 3 . (a) φ = 0.01, (b) φ = 0.03, and (c) φ = 0.05.

The discrepancy may suggest that the regulatory activity of AirR is strain specific. Why AirSR acts differently

in different strains is still not clear. Our speculation is that inactivation of sigma B in NCTC8325 may contribute to the different activity of AirSR in NCTC8325 and Newman. But this speculation needs further study. WalKR is an important TCS that positively controls cell wall biosynthesis and turnover, Tanespimycin including directly controlling lytM [12]. Alterations in the expression of WalKR as well as WalKR mutations at amino acid sequence can lead to a change in susceptibility to vancomycin [19, 30]. AirSR and WalKR exhibit similar functions. Our microarray data indicate that the WalKR expression level is unchanged in the airSR mutant, and there is no report so far that WalKR regulates AirSR, suggesting that the two TCSs

may regulate cell wall biosynthesis independently. see more Conclusions The airSR mutant exhibited reduced autolysis and down-regulation in many cell wall metabolism-related genes in S. aureus NCTC8325. And AirR can directly bind to the promoter region of some of these cell wall metabolism genes. These findings demonstrate that AirSR is a positive regulator in cell wall biosynthesis and turnover in S. aureus NCTC8325. The airSR mutant exhibited reduced viability in the presence of vancomycin, suggesting that AirSR could be a new target for controlling S. aureus infection. Acknowledgments The authors thank the Network on Antimicrobial TPX-0005 Resistance in Staphylococcus aureus (NARSA) for providing the bacterial strains. This study was supported

by the National Natural Science Foundation of China (grants 31070116 and 81371850). Electronic supplementary material Additional file 1: Correlationship between microarray data and the real-time RT PCR result. The transcriptional level of 11 genes from both microarray and real-time RT PCR were log2 transformed and plotted against each other. A linear fit analysis 2-hydroxyphytanoyl-CoA lyase was performed to check the correlation between the two methods. R2 = 0.9678. (TIFF 124 KB) Additional file 2: EMSA of cap promoter with unphosphorylated and phosphorylated AirR. The first lane was the free DNA probe (2 nM); the second to fourth lanes were the DNA probe with increasing amounts of unphosphorylated AirR (0.25, 0.5, and 1 μM); the fifth to seventh lanes were the DNA probe with increasing amounts of lithium potassium acetyl phosphate phosphorylated AirR (0.25, 0.5, and 1 μM); the eighth to tenth lanes were the DNA probe with increasing amounts of AirS phosphorylated AirR (0.25, 0.5, and 1 μM). (TIFF 145 KB) Additional file 3: Phylogenetic footprinting of AirR binding sequences.

Selected samples selleck screening library representative of the known diversity on Martha’s Vineyard were chosen to test new loci. If no variation was detected for a particular locus, it

was not pursued further. The VNTR loci used in this study Ispinesib chemical structure are: Ft-M3 (SSTR9), Ft-M10 (SSTR16), Ft-M2, Ft-M6, Ft-M8, and Ft-M9. All were amplified as previously described. [14, 15] The Ft-M2 locus had a high rate of amplification failures compared to the other loci tested. 16% of the FopA positive ticks successfully amplified all other loci but not Ft-M2. Ticks that had data from the other 3 loci were included in the diversity estimates that did not include the Ft-M2 locus. However, they were necessarily excluded in analyses that include the Ft-M2 locus. Both analyses are presented here. The number of repeat units for each locus SGC-CBP30 concentration was determined by comparing the obtained amplicon size with one that has a known number of repeats, such as Schu. VNTR haplotypes were then expressed as the number of repeat units. Some samples contained multiple peaks that were not likely to be stutter

peaks. These samples were scored as multiple alleles if the amplitude of the smaller peak was > 25% of the larger. These samples were then counted twice, once for each allele, in the MLVA. Simpson’s Index of Diversity was calculated as described previously. [22] eBurst Analysis The data from each field site was analyzed ADAMTS5 using eBURST http://​eburst.​mlst.​net/​. [23] eBURST displays the relationships between closely related samples from a bacterial population (e.g. [24, 25] It uses an algorithm to identify the founder of the population, by identifying the VNTR type that differs from more of the others by only one locus (single locus variants). It then predicts a likely evolutionary path by connecting VNTR types that differ by one locus and displays them as radial links to the founder. The confidence level for the founder is then calculated using 1000 bootstrap replicates. Population Structure Analysis The population structure of F. tularensis

tularensis on Martha’s Vineyard was analyzed using Multilocus http://​www.​agapow.​net/​software/​multilocus/​. [26] Samples from Squibnocket and Katama were tested to determine whether there was linkage disequilibrium among the loci by calculating the index of association. Randomized datasets (100) that shuffle the alleles among individuals, independently for each locus, were compared to the observed data to calculate statistical significance (set a priori at P < 0.05). Evidence for differentiation between the two populations was found using Weir’s formulation of Wright’s Fst for haploids. Randomizations were used to calculate significance for this statistic also. In this case the observed data was compared to datasets of the individuals randomized across populations.

2), the non-relaxed fraction of quantum yield after 30 min in dark (q i) was 0.30 ± 0.04 in the sun leaves and 0.39 ± 0.07 in the shade leaves. Increase

of relative variable fluorescence at 2 ms (V J) indicates stronger limitation of KU-60019 electron transport from QA to QB as shown also numerically by the values of probability (ψET2o) of trapped PSII electron transfer from reduced QA to QB (Table 4). The variable Chl fluorescence increase from I to P represents the measure of electron transport from QB beyond PSI (Munday and Govindjee 1969; Schansker et al. 2003). As is evident by the values of the probability with which the electron moves toward H 89 solubility dmso PSI end acceptors, ψRE1o, the electron transport between PSII and PSI after HL treatment becomes selleck screening library less limited (Table 4), especially in shade leaves. (For a detailed discussion on the interpretation of the J–I–P rise (the so-called thermal phase of fast ChlF kinetics), see a review by Stirbet and Govindjee 2012). Another explanation for the above results is that HL treatment affects the post-illumination redox state of the PQ pool, and the activation state of the PS I acceptor side (e.g., due to FNR activity) probably does not decay within the 30-min dark period that was used before the measurements. Stromal

components can donate electrons to the PQ pool in the dark. Reduction in the dark can be substantially stimulated by pre-illumination with strong light (Asada et al. 1992). An increase of PQ-pool reduction with respect to the control will induce an increase of the J-step (Toth et al. 2007) and, hence, of all the parameters based on the values of V J. This

is also supported by increased values of F 0 in samples 30 min after HL treatment. The changes of connectivity parameters (p 2G, p, ω) after HL treatment were mostly insignificant (Table 4); moreover, according to Laisk and Oja (2013), estimates of p parameter can be strongly influenced by the redox status of the PQ pool. Since F 0 value may increase in samples after HL treatment, calculated values of connectivity parameters may not be used as a measure of true PSII connectivity. Nevertheless, the insignificant differences between the F 0 values Masitinib (AB1010) before and after HL treatment and the maintained significance of differences between the sun and shade leaves suggest that the estimate of connectivity parameters could not be as prone to errors due to PQ redox status as expected. The membrane model parameters (Table 4) show energy flux parameters per active RC. A higher value of the inferred absorbance per RC (ABS/RC) in shade leaves before HL treatment (~2.6) as compared to the sun leaves (~2.2) seems to indicate increased antenna size per active RC (Strasser et al. 2000; Stirbet and Govindjee 2011). However, a correction for connectivity (Suppl. Table 2; see information given in parentheses), i.e., multiplying the ABS/RC by 1 + C where C is the curvature constant of the relative variable fluorescence curve (Force et al.

bacteriovorus HD100 attached to, invaded and killed P. tolaasii 2192T cells by forming bdelloplasts on the pileus surface, when added both before or after P. tolaasii 2192T inoculation (Figure 3d and e); thus, reduction in P. tolaasii 2192T numbers and disease symptoms was due to predatory activity by B. bacteriovorus HD100. As the consumer preference is for white, clean-looking mushrooms with minimal surface damage, the reduction in brown

blotch tissue LDN-193189 damage by B. bacteriovorus application could increase the yield and possibly the shelf life of high-quality, marketable mushrooms. This study investigated the survival of B. bacteriovorus HD100 and its predatory activity against P. tolaasii on the surface of post-harvest mushrooms up to 48 hours, sufficient time for brown blotch disease to develop on untreated mushrooms. Thus studies over longer time points, covering Torin 2 research buy time from transportation to the sell-by learn more date, would need to be investigated, in future work, if Bdellovibrio was to be applied as a treatment to extend shelf-life. In addition to reducing the population of P. tolaasii on the mushroom surface, Bdellovibrio are natural soil dwellers and so their application to casing soil could also prevent spread of brown blotch between mushrooms in the growth environment and between grow houses.

In this way, the fast swimming motility of Bdellovibrio [38] would allow efficient location of P. tolaasii prey, using chemotaxis, in the wet casing soil prior to mushroom growth initiation, and translocation by gliding along the mushroom pileus surface after mushroom fruiting bodies have formed, preventing P. tolaasii infection establishment at multiple stages of mushroom growth; previously, the possibility of infection throughout the mushroom growth period has been an obstacle in brown blotch disease

control. Further pre-harvest studies could investigate the longevity and protective effect of Bdellovibrio inoculated into the casing soil around mushroom mycelium, before Mannose-binding protein-associated serine protease and after fruiting body initiation, on growing A. bisporus. As Bdellovibrio preys efficiently upon some, but not all, species of Pseudomonas (unpublished observations), and some Pseudomonads in the casing soil such as P. putida are important in fruiting body initiation; further studies would additionally investigate the predatory activity of B. bacteriovorus HD100 against such commensal strains in vitro and in the casing soil to ensure that there are no effects that would have an adverse impact on mushroom fruiting body production. As host-dependent Bdellovibrio require prey cells to survive, the post-harvest treatment could also be self-limiting, as Bdellovibrio would die once P. tolaasii prey had been eradicated; further studies could quantify this. Furthermore, these in vitro and in vivo predation studies suggest that B. bacteriovorus may be able to survive the action of the toxins produced by P.

References 1. Ludwig KA, Quebbeman EJ, Bergstein JM, Wallace JR, Wittmann

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W, De Keyser J, Brabant S, Spoelders K, Vuylsteke P, Beeusaert R, Coppe E: Colon ischaemia and necrosis as a complication of prolonged but successful CPR. Resuscitation 2006, 71:260–262.PubMedCrossRef 11. Jaeckle T, Stuber G, Hoffmann MHK, Freund W, Schmitz BL, Aschoff AJ: Acute gastrointestinal bleeding: Value of MDCT. Abdom Imaging 2008, 33:285–293.PubMedCrossRef 12. Wiesner W, Khurana B, Ji H, Ros PR: CT of acute bowel ischemia. Radiology 2003, 226:635–650.PubMedCrossRef 13. Horton KM, Fishman EK: Multidetector CT angiography in the diagnosis of mesenteric ischemia. Radiol Clin North Am 2007, 45:275–288.PubMedCrossRef 14. Nikas D, Ahn Y, Fielding LP: Sensitivity of colon

mafosfamide blood flow to changing haemorrhagic events. Curr Surg 1985, 42:20–23.PubMed 15. Bailey RW, Bulkley GB, Hamilton SR, Morris JB, Smith GW: Pathogenesis of non-occlusive ischemic colitis. Ann Surg 1986,203(6):590–599.PubMedCrossRef 16. Toung T, Reilly PM, Fuh KC, Ferris R, Bulkley GB: Mesenteric vasoconstriction in response to hemorrhagic shock. Shock 2000,13(4):267–273.PubMedCrossRef 17. Reilly PM, Wilkins KB, Fuh KC, Haglund U, Bulkley GB: The mesenteric hemodynamic response to circulatory shock: an overview. Shock 2001,15(5):329–343.PubMedCrossRef 18. Ceppa EP, Fuh KC, Bulkley GB: Mesenteric hemodynamic response to circulatory shock. Curr Opin Crit Care 2003,9(2):127–132.PubMedCrossRef 19. Chou CK: CT manifestations of bowel ischaemia. AJR 2002, 178:87–91.PubMed 20.

A P value <0.05

was considered to indicate a significant difference. Results and discussions Synthesis and characterization of Lenvatinib mouse PLA-PCL-TPGS random copolymer. The structure of the synthesized PLA-PCL-TPGS copolymer was detected by 1H NMR in CDCl3. Figure 1 shows the chemical structure of PLA-PCL-TPGS random copolymer and 1H NMR spectroscopy of the PLA-PCL-TPGS copolymer. The signals at 5.2 and 1.69 ppm (peaks a and e) were assigned to the CH protons and methyl protons -CH3 of PLA segment, respectively. The peak at 3.65 ppm (peak c) was assigned to the -CH2 protons of PEO part of Q-VD-Oph ic50 TPGS. The lower peaks in the aliphatic region belong to various moieties of vitamin E tails. The peaks at 4.06 (peak b), 2.31 (peak d), 1.60 to 1.70 (peak e), and 1.35 to 1.43 (peak f) were assigned to -OCH2, -COCH2, -CH2 (4 H), and -CH2 (2 H) segments of PCL, Fosbretabulin clinical trial respectively [24]. The molecular weight of the PLA-PCL-TPGS was calculated using the ratio between the peak areas at 4.06 (peak area 9.64), 5.2 (peak area 1.23), and 3.65 (peak area 3.00). The number-averaged molecular weight of the PLA-PCL-TPGS random copolymer was determined to be 33,229. The feeding ratios of ε-caprolactone, lactide, and TPGS molecular mass were 75%, 15%, and 10%, respectively. However, the ratios of ε-caprolactone, lactide, and TPGS molecular mass

which were integrated into the PLA-PCL-TPGS copolymers were 87.18%, 8.17%, and 4.64%. Characterization of nanoparticles Size, zeta potential, and encapsulation efficiency The particle size data of the 5% thiolated chitosan-modified PCL nanoparticles (CNP), unmodified PLA-PCL-TPGS nanoparticles (UNP), 5% thiolated chitosan-modified PLA-PCL-TPGS nanoparticles (TNP), and 20% thiolated chitosan-modified PLA-PCL-TPGS nanoparticles (DNP) fabricated in this new research are presented in Table 1. The particle size was found to be an important parameter regarding particle uptake. The small nanoparticle size may provide a large surface area and increase in mucin adsorption, which leads to a high mucoadhesive property

for the nanoparticles [34]. The permeability of the particles through the intestinal mucosa decreases with increasing particle size reaching a cut-off at around 500 nm [35, 36]. The average diameter of the resulted nanoparticles was around 200 nm, which is in the size range favoring the intestinal uptake of the nanoparticles [2, 8]. The results also showed that the addition of thiolated chitosan resulted in a slight increase in particle size. Zeta potential analysis confirmed that surface modification with 5% thiolated chitosan reversed the PLA-PCL-TPGS nanoparticles from a negative surface charge of −18.29 mV to a significantly positive charge of +24.66 mV. As reported in the literature, positive surface charge could enhance the mucosal uptake due to anionic nature of mucous layer [37].