The extracellular matrix SN-38 order surrounded the entire cell except for the inside lining of the vestibulum, which leads to the flagellar pocket and feeding pockets EPZ015938 (Figures 2C, 3D-E). The portion of the extracellular matrix positioned just inside the opening

of the vestibulum lacked epibiotic bacteria and consisted of fine hair-like structures, or somatonemes (Figure 3E). The extracellular matrix beneath the epibiotic bacteria was coated with a thin glycocalyx (Figures 4B-D, 5). The extracellular matrix itself was bright orange, approximately 100 nm thick and perforated with hollow tubes that joined the plasma membrane of the host with the glycocalyx beneath the epibiotic bacteria (Figures 1G, 4A-C, 5). Figure 4 Transmission electron micrographs (TEM) showing the surface ultrastructure of Calkinsia aureus. A. Tangential TEM section showing

conduit-like perforations (arrowheads) embedded within the extracellular matrix (Ex), an array of microtubules, and mitochondrion-derived organelles (MtD). (bar = 1 μm). B. Mitochondrion-derived organelles (MtD) with two membranes (arrow) above the ER. The convoluted appearance of the cell plasma membrane (double arrowhead) and a longitudinal view of a microtubule (arrowhead) are also shown. A glycocalyx (GL) covers the surface of the extracellular matrix (Ex). C. Transverse TEM showing the epibiotic bacteria (B), the glycocalyx (GL), a conduit-like perforation (arrow) through the extracellular matrix (Ex) and the underlying sheet Lazertinib manufacturer of microtubules (B, C, bars = 500 nm). D. High magnification view showing the epibiotic bacteria (B), the glycocalyx (GL), the extracellular Benzatropine matrix (Ex), the cell plasma membrane (double arrowhead), and the double-layered structure (arrowhead; derived from the dorsal lamina) beneath a sheet of inter-connected microtubules (bar

= 200 nm). E. Mitochondrion-derived organelles (MtD) (bar = 500 nm). Inset: High magnification TEM showing the two membranes that surround the mitochondrion-derived organelles (width of inset = 400 nm). Figure 5 Diagram of the cell surface of Calkinsia aureus. The diagram shows epibiotic bacteria (B), the glycocalyx (GL), the perforated extracellular matrix (Ex), the host cell plasma membrane (double arrowhead), the linked microtubules (LMt), the double-layered structure (arrowhead), mitochondrion-derived organelles (MtD) and cisternae of endoplasmic reticulum (ER). An array of evenly spaced microtubules was positioned immediately beneath the plasma membrane of the host (Figures 4A, 4C-D, 5). These microtubules were derived from the dorsal lamina (DL) of the flagellar apparatus (see description below).

Bott M: Anaerobic citrate FG 4592 metabolism and its regulation in enterobacteria. Arch Microbiol 1997, 167:78–88.CrossRef 3. Kaspar S, Perozzo R, Reinelt S, Meyer M, Pfister K, Scapozza L, Bott M: The periplasmic domain of the histidine autokinase CitA functions as a highly specific citrate receptor. Mol Micorbiol 1999, 33:858–972.CrossRef 4. Meyer M, Dimroth P, Bott M: Catabolite repression of the citrate fermentation genes in Klebsiella pneumoniae : Evidence for involvement of cyclic AMP receptor protein. J Bacteriol 2001, 183:5248–5256.CrossRefPubMed

5. Bott M, Meyer M, Dimroth P: Regulation of anaerobic citrate selleck products metabolism in Klebsiella pneumoniae. Mol Microbiol 1995, 18:533–546.CrossRefPubMed 6. Meyer M, Dimroth P, Bott Small molecule library cell line M: In vitro binding of the response regulator CitB and of its carboxy-terminal domain to A + T-rich DNA target sequences in the control region

of the divergent citC and citS operons of Klebsiella pneumoniae. J Mol Biol 1997, 269:719–731.CrossRefPubMed 7. Schneider K, Kästner CN, Meyer M, Wessel M, Dimroth P, Bott M: Identification of a gene cluster in Klebsiella pneumoniae which includes citX , a gene required for biosynthesis of the citrate lyase prosthetic group. J Bacteriol 2002, 184:2439–2446.CrossRefPubMed 8. Johnson JR: Virulence factors in Escherichia coli urinary tract infection. Clin Microbiol Rev 1991, 4:80–128.PubMed 9. Bergsten G, Wullt B, Svanborg C:Escherichia coli , fimbriae, bacterial persistence and host response induction in the human urinary tract. Int J Med Microbiol 2005, 295:487–502.CrossRefPubMed 10. Purcell BK, Clegg S: Construction and expression of recombinant Janus kinase (JAK) plasmids encoding type 1 fimbriae of a urinary Klebsiella pneumoniae isolate. Infect Immun 1983, 39:1122–1127.PubMed 11. Jones CH, Pinkner

JS, Roth R, Heuser J, Nicholes AV, Abraham SN, Hultgren SJ: FimH adhesin of type 1 pili is assembled into a fibrillar tip structure in the Enterobacteriaceae. Proc Natl Acad Sci USA 1995, 92:2081–2085.CrossRefPubMed 12. Wu KM, Li LH, Yan JJ, Tsao N, Liao TL, Tsai HC, Fung CP, Chen HJ, Liu YM, Wang JT, Fang CT, Chang SC, Shu HY, Liu TT, Chen YT, Shiau YR, Lauderdale TL, Su IJ, Kirby R, Tsai SF: Genome sequencing and comparative analysis of Klebsiella pneumoniae NTUH-K a strain causing liver abscess and meningitis. J Bacteriol 2044, 191:4492–4501.CrossRef 13. Chou HC, Lee CZ, Ma LC, Fang CT, Chang SC, Wang JT: Isolation of a chromosomal region of Klebsiella pneumoniae associated with allantoin metabolism and liver infection. Infect Immun 2004, 72:3783–3792.CrossRefPubMed 14. Fouts DE, Tyler HL, DeBoy RT, Daugherty S, Ren Q, Badger JH, Durkin AS, Huot H, Shrivastava S, Kothari S, Dodson RJ, Mohamound Y, Khouri H, Roesch LF, Krogfelt KA, Struve C, Triplett EW, Methé BA: Complete genome sequence of the N2-fixing broad host range endophyte Klebsiella pneumoniae 342 and virulence predictions verified in mice. PLoS Genet 2008, 4:e1000141.CrossRefPubMed 15.

The check details reaction products were separated by thin layer chromatography, and quantified as described in the experimental procedures. Data are from three independent measurements and are presented as mean ± SD. Table 4 Kinetic parameters of trifluorothymidine with purified recombinant human TK1, TK2, and Ureaplasma TK*   Km(μM) kcat(s-1) kcat/Km(s-1M-1)×103

Human TK1 5.9 ± 1.7 0.043 ± 0.003 7.3 ± 1.8 Human TK2 8.8 ± 3.8 0.026 ± 0.003 3.0 ± 0.8 Ureaplasma TK 9.9 ± 5.2 0.055 ± 0.008 5.6 ± 1.5 *Assays were performed using phosphoryl transfer assay with [γ-32P]-labelled ATP (100 μM) and variable concentrations of TFT (1 – 100 μM). The reaction products were separated by thin layer chromatography and were quantified. Thymidine (10 μM) Selleckchem THZ1 was used as a control. Data are from three independent measurements and are expressed as mean ± SD. Inhibition of human TK1, TK2, and Ureaplasma and Mpn TK by TFT and 5FdU Both TFT and 5FdU are substrates of Mycoplasma and human TKs, as described above and earlier studies [30, MGCD0103 supplier 40, 41]. However, their inhibitory effects

on these enzymes are not known, and inhibition of TK activity by these two analogs may account for the observed Mpn growth inhibition. Therefore, we determined the IC50 values for TFT and 5FdU with dT as a substrate and found significant differences in IC50 values between TFT and 5FdU for all enzymes. TFT inhibited dT phosphorylation in Mpn protein extracts with an IC50 value of 9.1 ± 2.9 μM, which was similar to that of recombinant

Ureaplasma TK. With recombinant human TK1 and TK2, the IC50 values were 9.7 ± 3.2 μM and 80 ± 5.6 μM, respectively. The inhibition by 5FdU was much weaker for all recombinant enzymes and Mpn extracts (Table 5). Thus, TFT was a significantly better inhibitor than 5FdU. Table 5 IC 50 values (μM) of trifluorothymidine (TFT) and 5-fluorodeoxyuridine (5FdU) with purified recombinant human TK1 and TK2, Ureaplasma TK, and Mpn extracts *   TFT 5FdU P value Human TK1 9.7 ± 3.2 75.9 ± 2.6 <0.0001 Human TK2 80 ± 5.6 158.5 ± 2.7 <0.0001 Ureaplasma TK 12.0 ± 4.2 1000 ± 13.3 <0.0001 Mpn extracts 9.1 ± 2.9 47.9 ±1.2 <0.0001 *Assays were performed with 10 μM tritium labelled thymidine as substrate in the presence of various concentrations 17-DMAG (Alvespimycin) HCl of the inhibitors. Data were mean ± SD from at least three independent determinations. P value < 0.05 is considered as significant. Discussion Mycoplasmas differ from their hosts in the biosynthesis of precursors for DNA and RNA because they cannot synthesize purine and pyrimidine bases de novo. Therefore, they rely totally on the salvage pathway for nucleotide biosynthesis (depicted in Figure 4). Purine bases such as Hx, Gua, and Ade are recycled by HPRT and adenine phosphoribosyl transferase, whereas the pyrimidine base, uracil is salvaged by uracil phosphoribosyl transferase [31, 32]. The salvage of deoxynucleosides is catalyzed by deoxynucleoside kinases, including TK and deoxyadenosine/deoxyguanosine kinase [29].

J774A.1 macrophages were exposed to Burkholderia strains at an MOI of 10 and the mean numbers of intracellular

bacteria were determined at 2, 4, 6, 8 and 12 hrs post infection. (A) Uptake of bacteria by macrophages as determined by bacterial counts 2 hrs post infection relative to the input numbers. (B-D) Intracellular survival and replication of B. pseudomallei (Bps; panel B), B. Z-IETD-FMK purchase thailandensis (Bt; panel C) and B. oklahomensis (Bo; panel D) in J774A.1 macrophage cells. Error bars represent the standard CP-690550 cost error of the mean. All infections were performed as three independent experiments, each with three technical replicates. The insert in panel C represents individual bacterial counts and the mean value at 12 hrs post infection with different B. thailandensis strains. High virulence isolates of B. pseudomallei grow more rapidly in J774A.1 macrophages than low virulence isolates, B. thailandensis or B. oklahomensis Next, intracellular replication was measured at 2, 4, 6, 8 and 12 hrs post infection. There was a significant difference between the numbers of intracellular

B. pseudomallei strains 576 and K96243 at 12 hrs post infection (P = 0.002; Figure 1B) and both were significantly higher than numbers of intracellular B. pseudomallei strain 708a and any of the B. thailandensis or B. oklahomensis strains tested (P < 0.002, both). Bacterial numbers were over 10-fold click here lower with any of the B. thailandensis or B. oklahomensis strains tested (compare Figure 1B to Figure 1C & 1D). To test whether the low numbers of intracellular bacteria observed with B. pseudomallei 708a, which is more sensitive to kanamycin, was a consequence of low levels of antibiotic crossing the eukaryotic cell membrane, J774A.1 cells were infected with B. thailandensis DW503 (an amrAB-oprA efflux pump mutant and therefore highly

sensitive to kanamycin) and intracellular bacterial numbers were compared to its parental strain E264. The numbers of bacteria isolated at each time point were not significantly different between strains E264 and DW503 (data not shown). Our results also showed variance between the patterns of growth in macrophages of different isolates of B. thailandensis. The B. thailandensis strains previously isolated from cases 5-FU mw of human disease, CDC272 and CDC301, showed increased numbers at 12 hrs post infection relative to B. thailandensis E264 (P < 0.004, both; see insert in Figure 1C) and the two B. oklahomensis strains C6786 and E0147 (P < 0.009, both), but not B. thailandensis strain Phuket (P > 0.05). To show that these differences in bacterial numbers were due to differences in intracellular replication and survival rather than a difference in bacterial fitness, growth rates of bacteria in antibiotic free media were compared. There was no significant difference between any of the strains tested (data not shown).

In fact, such proteins may have been the result of simple condensation reactions of amino acids, these reactions were probably DNA independent and so their products were short random polypeptides. Of course, similar molecules Selleckchem MK-1775 are far away from having the properties of enzymes but may have been the original population from which are then emerged the natural proteins. A characteristic certainly indispensable for the catalytic activity is the three-dimensional structure. From this evidence was born the idea that the folding could have been an important factor of discrimination between prebiotic polypeptides; chains able to have a stable fold are more soluble in water and more resistant to hydrolysis,

have a greater “fitness” than other and could therefore QNZ nmr have been naturally selected for this feature. For these reasons, our interest is focused on short random polypeptide sequences, these are in fact much more resemble natural proteins to those who may have been the first enzymes that were formed on our planet. To discriminate folded proteins against the unstable ones it was decided to subject the library of sequences

produced by Phage Display to enzymatic digestion. The polypeptides were designed to contain in the middle of the random sequence the PRG residues, substrate recognized by the protease Thrombin. In this way it is possible to distinguish those proteins inside the library that are resistant to enzyme from those that are digested. The resistant proteins have probably a tertiary structure that makes the PRG site inaccessible to protease. The library was further tested by subjecting sequences of interest to other proteolytic non specific enough enzymes such as trypsin and chymotripsine. The activity of these proteases is influenced by the nature of tertiary structure of the protein substrate, therefore the analysis of the digestion products can highlight the formation of particularly stable structures. The Small molecule library interested polypeptides were subjected to enzymatic digestion for various time intervals and with different protease concentrations. Cyclical steps of this procedure were resulted to select, inside the

library, the more resistant sequences, the ones that may to have a stable tertiary structure and thus may have potentially some kind of biological activity. The investigation of 79 sequences, randomly selected from the initially large library, shows that over 20% of this population is thrombin-resistant, likely due to folding. Analysis of the amino acid sequences of these clones shows no significant homology to extant proteins, which indicates that they are indeed totally de novo. The DNA sequences coding the corresponding resistant proteins were cloned into appropriate vectors, expressed in E. coli and then purified and analyzed in order to determine the tertiary structure and assess the chemical and physical characteristics.

Only a slight difference in band richness was found between the time points of the study (T0, mean of bands: 15.8; T1, mean of bands: 14.8). DGGE bands were subjected to Mann-Whitney U-test in order to search for significant differences in the intensities between T0 and T1. No band showed a significant

variation, indicating that the consumption of the synbiotic food did not alter the concentration of any major species of intestinal find more microbiota. Pearson correlation was used to calculate the similarity index (SI) between DGGE band profiles related to the time points T0 and T1 for each healthy volunteer (Table 1). The high median value of SI (67.1%) revealed that the dominant bacterial composition remained PF-01367338 solubility dmso constant over the treatment. Only 3 subjects presented SIs lower than 50% (subjects 8, 12 and 20). No subject showed significant variations between selleck compound DGGE band profiles related to T0 and T1, as evaluated using the Pearson correlation analysis (P > 0.05). Table 1 Similarity index (SI) of DGGE profiles related to T0 and T1 Subject SI (%) 1 71.8 2 60.6 3 79.2 4

54.1 5 91.3 6 55.9 7 77.5 8 47.7 9 65.0 10 89.3 11 80.9 12 38.2 13 76.1 14 64.7 15 66.6 16 59.4 17 80.3 18 64.3 19 72.1 20 46.4 Figure 1 DGGE analysis of the fecal samples recovered from 20 healthy volunteers (s1-s20) before (T0) and after (T1) one month of the synbiotic intake. A: DGGE profiles related to fecal samples and L. helveticus Bar13 and B. longum Bar33 probiotic strains. B: line graph. C: Cluster analysis (Pearson correlation was used to calculate the similarity in DGGE profiles). Cluster analysis of DGGE population profiling confirmed the stability of the overall

structure of the microbiome, revealing no grouping according to the feeding (Figure 1B-C). T0 and T1 banding patterns were closely related for all the volunteers, except for the subject 8 (SI: 47.7%). Among different subjects, considerable variation in the composition of the population fingerprints could be observed. Both qualitative (presence or absence of a band) or quantitative (variable intensity of a band) variations did occur. These inter-individual variations were N-acetylglucosamine-1-phosphate transferase higher than changes elicited by the functional food consumed. Quantitative variations of bifidobacteria and lactobacilli In order to evaluate the effect of the prebiotic component on modulation of bifidobacteria and lactobacilli populations and the capability of the probiotic bacteria to pass through the gut of the healthy host, quantitative variations of Bifidobacterium and Lactobacillus genera were determined by real-time PCR and compared to the variations of the species B. longum and L. helveticus (Table 2). All volunteers naturally harbored strains belonging to Bifidobacterium and Lactobacillus, as demonstrated by the presence of these genera in all stool samples recovered before the beginning of the feeding trial. B. longum was also found in all healthy subjects at the time point T0, in accordance with previous studies reporting B.

2008), with the most common genera comprising Cryptosphaeria Ces. & De Not., Cryptovalsa (Ces. & De Not.), Diatrype Fr., Diatrypella (Ces. & De Not.) De selleck inhibitor Not., Eutypa Tul. & C. Tul., and Eutypella (Nitschke) Sacc. While several species, such as Cryptovalsa ampelina (Nitschke) Fuckel, Eutypa lata (Pers.: Fr.) Tul. & C. Tul. and E. leptoplaca (Mont.) Rappaz, are cosmopolitan (Carter 1991; Trouillas and Gubler 2004; Trouillas et al. 2010a, b), others, most notably Diatrype disciformis (Hoffm. : Fr.) Fr. are thought be extremely rare outside Europe (Rappaz 1987). Furthermore, some species appear to be associated with a specific host, for instance Eutypa maura (Fr. : Fr.)

Fuckel on Acer pseudoplatanus (Rappaz 1987), while others, specifically E. lata, E. leptoplaca and C. ampelina demonstrate wider host ranges (Carter et al. 1983; Rappaz 1987; Trouillas and Gubler 2004; Trouillas and Gubler 2010; Trouillas et al. 2010a, ATM Kinase Inhibitor purchase b). Regardless, species within the Diatrypaceae have, for the most part, been considered saprotrophic, although some species appear to be selleck chemical especially well established in the wood of recently dead host plants (Tiffany and Gilman 1965). Nevertheless, a few species in this family are known as severe plant pathogens of woody crops, landscape and forest trees in the United States (US) and Europe (Carter 1957; Carter 1991; Davidson and Lorenz 1938; Hinds and Laurent 1978; Hinds 1981; Moller and Kasimatis 1978;

Munkvold and

Marois 1994; Sinclair and Lyon 2005; Jurc et al. 2006). Among those of economical importance, E. lata has been studied extensively both in Australia and around the world as the causal agent of Eutypa dieback of grapevine (Vitis vinifera L.) and apricot (Prunus armeniaca L.) (Carter 1957; Carter 1991). The biodegradation potential of diatrypaceous strains was recently investigated (Pildain et al. 2005). This study has shown that some members of the Diatrypaceae family produce cellulase and lignin-degrading enzymes, extracellular enzymes that catalyse the hydrolysis of cellulose and breakdown of lignin in the cell walls of plants, thus affording some species the physiological capacity to produce wood decay (Pildain et al. 2005). Recent studies in the US reported several species as putative pathogens of grapevine (Rolshausen et al. 2004; Catal et al. 2007; see more Trouillas and Gubler 2004; Trouillas and Gubler 2010; Trouillas et al. 2010a, b; Úrbez-Torres et al. 2009). Eutypella vitis (Schwein.:Fr.) Ellis and Everh. [syn.: E. aequilinearis (Schwein.:Fr.) Starb.] and Diatrypella sp. were shown to be somewhat pathogenic to grapevine in Texas (Úrbez-Torres et al. 2009). In California, E. leptoplaca, Diatrype stigma (Hoffm. : Fr.) Fr., D. whitmanensis J.D. Rogers & Glawe, Cryptosphaeria pullmanensis Glawe and C. ampelina were shown to infect grapevine wood, causing decay of vascular tissues (Trouillas and Gubler 2004; Trouillas and Gubler 2010).

Limitations in operating room (OR) resources may also Alpelisib hinder the expedited delivery of care for emergency patients [10, 11]. Traditionally, on-call surgeons YM155 would either cancel their elective caseload to accommodate emergency surgeries, or delay operating on the emergency patient until they had elective OR time [12–14]. To mitigate this issue, acute care surgery (ACS) services have been widely adopted as a cost-effective model for delivering emergency surgical care [12–14]. ACS teams provide around-the-clock coverage to manage patients with all types of general surgical emergencies [14]. They have been

shown to significantly reduce wait-times for urgent and emergent operations [15–18], expedite the efficient disposition of patients from the emergency room [15–18], and reduce hospital costs [11, 16] without compromising patient care or safety [19]. However, the management of diseases which are commonly encountered selleck compound by ACS services do not usually require

long-term surveillance for disease recurrence [16, 20]. The acute care of emergency CRC patients therefore presents a relatively more complex challenge as it requires the coordination of multiple specialties, including gastroenterologists, surgeons, and oncologists (medical and/or radiation) [2, 3, 5, 8]. While ACS services in the United States are typically staffed by subspecialty trauma and acute care surgeons [19, 20], many Canadian ACS teams are run by surgeons who also routinely perform cancer operations as part of their elective practices [14, 21]. We, therefore, sought to assess whether the

implementation of the Acute Care and Emergency Surgery Service (ACCESS) at our institution would expedite the surgical treatment of emergency CRC patients. Rather than assess the surgical management of emergency CRC per se, we elected to focus our study on the delivery of care for these patients. Methods Ethics approval for this study was obtained through the Western University Research and Ethics Board (REB Number 102988). This study was conducted at the London Health Sciences Centre (LHSC), a tertiary-care hospital system with two university-affiliated institutions serving a metropolitan Florfenicol population of approximately 450,000. Additionally, the two centres receive referrals from 33 regional hospitals from 7 counties, covering a catchment area of 3 million [22]. Both hospitals within LHSC perform a high volume of colorectal cancer surgeries: University Hospital (UH), which lacks an ACS service (non-ACCESS), and Victoria Hospital (VH), where ACCESS was implemented in July 2010. The two sites function relatively independently, with no crossover of surgical consultants or gastroenterologists. At VH, all surgeons who participate in ACCESS also perform colorectal cancer operations as part of their elective practices.

These results suggested that polymorphisms at rs2280883 within the FOXP3 gene may be Tanespimycin mw associated with idiopathic infertility, while polymorphisms at rs3761549 may be related to endometriosis. However, it remains unclear whether FOXP3 gene polymorphism is associated with hepatitis B-related HCC. Based on FOXP3 gene SNP genotype data from the HapMap Phase II + Phase III database, two

tagSNPs, rs2280883 and rs3761549, were selected for genotyping because these two SNPs could cover 80% of the MAF > 0.1 SNPs. To investigate the correlation between specific SNPs in the FOXP3 gene and hepatitis B-related HCC, Matrix-Assisted Laser Desorption/Ionization Time of Flight (MALDI-TOF) Mass Spectrometry was used to screen for the presence of the FOXP3 gene polymorphisms in HCC donors, CHB donors and healthy donors. Here, we present data describing Selleck STI571 an association between FOXP3 genetic variation and susceptibility to hepatitis B-related HCC in all donors. Materials and methods Study subjects and peripheral blood samples Peripheral blood samples were obtained from 392 HCC patients, 344 CHB patients and 372 healthy donors. HCC patients were treated at the Guilin Medical University-affiliated hospital between November 2001 and April 2010. CHB patients with diagnoses

conformed to the buy CH5183284 latest diagnostic criteria [20] were from the Peking University Hepatology Institute (Peking, China) between November 2001 and April 2010. Healthy donors were patients undergoing routine physical examination at Peking University People’s Hospital. General patient information was Morin Hydrate recorded in detail, including age, gender, alcohol abuse, cirrhosis, presence of hepatitis B or hepatitis C virus (HCV) infection, alpha-fetoprotein (AFP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transpeptidase (GGT) and total bilirubin (TBIL) levels; this information is

provided in Table 1. HCC patient information, such as primary tumor size, histologic tumor type, histologic grade, lymph node (LN) stage, portal vein thrombosis and distant metastasis, were routinely assessed according to the TNM staging criteria proposed in 2002 by the International Union against Cancer (UICC) and American Joint Committee on Cancer (AJCC). All CHB patients have been screened by B-ultrasound and CT examination to exclude cancers. Healthy donors were selected at random; none had HBV and HCV infection according to screening for HBsAg and anti-HCV, and donors with liver cirrhosis or tumor-related diseases were excluded by B-ultrasound and CT examination. The study was implemented after receiving the approval of the Medical Ethics Committee of Peking University People’s Hospital. Written informed consent was obtained from all patients prior to sample collection according to the Declaration of Helsinki in 1995 (as revised in Tokyo, 2004).

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