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of progressive multiple sequence alignment through sequence weighting, position-specific gap penalties and weight matrix choice. Nucleic Acids Res 1994, 22:4673–4680.PubMedCrossRef 29. Keller A, Nesvizhskii A, Kolker E, Aebersold R: Empirical statistical model to estimate the accuracy of peptide identifications made by MS/MS and database search. Anal Chem 2002, 74:5383–5392.PubMedCrossRef 30. Nesvizhskii A,

Keller A, Kolker E, Aebersold R: A statistical model for identifying proteins by tandem mass spectrometry. Anal Chem 2003, 75:4646–4658.PubMedCrossRef 31. Silva J, Denny R, Dorschel C, Gorenstein M, Li G-Z, Richardson K, Wall D, Geromanos S: Simultaneous qualitative and quantitative analysis of the Escherichia coli proteome: a sweet tale. Mol Cell Proteomics 2006, 5:589–607.PubMed 32. Geromanos S, Vissers JPC, Silva FER J, Dorschel C, Li G-Z, Gorenstein M, Bateman R, Langridge J: The detection, correlation, and comparison of peptide precursor and product ions from data independent LC-MS with data dependant LC-MS/MS. Proteomics 2009, 9:1683–1695.PubMedCrossRef Authors’ contributions RT helped with the experimental design, carried out experiments, data preparation and in silico proteomics analysis, created dendrograms and drafted the manuscript. HM initiated the project, conceived the whole study and experimental design, carried out experiments and contributed to interpretation and writing. AW contributed intellectually to experimental design, data analysis, bioinformatics and manuscript review. JR, DS and JB contributed intellectually to experimental design, data analysis, and manuscript review. All authors read and approved the final manuscript.

Four different intimin types were identified: θ2 (theta), σ (sigma), τ (tau) and upsilon (Table 1). We have detected in aEPEC strains 4281-7 and 1632-7 (serotypes O104:H- and O26:H-, respectively)

two new intimin genes eae-τ and eae-ν that PND-1186 chemical structure showed less than 95% nucleotide sequence identity with existing intimin genes. Furthermore, a third new variant of the eae gene (theta 2 – θ2) was identified find more in the aEPEC strain 1871-1 (serotype O34:H-). The complete nucleotide sequences of the new eae-θ2 (FM872418), eae-τ (tau) (FM872416) and eae-upsilon; (FM872417) variant genes were determined. By using CLUSTAL W [41] for optimal sequence alignment, we determined the genetic relationship of the three new intimin genes and the remaining 27 eae variants. A genetic identity of 90% was calculated between the new eae-τ (tau) variant and eae-γ2 (gama2),

eae-θ (theta) and eae-σ (sigma) genes. The eae-upsilon; showed a 94% of identity with eae-ι1. The eae-θ2 (theta-2) gene is very similar (99%) to eae-θ of Tarr & Whittam [20] and to eae-γ2 of Oswald et al. [19]. Table 1 Characteristics of the aEPEC strains studied. Strain Serotype Intimin Type Adherence pattern FAS test         HeLa cells T84 cells 0621-6 ONT:H- σ * LA + + 1551-2 ONT:H- ο LA + + 1632-7 O26:H- upsilon; ** DA + + 1871-1 O34:H- θ2 ** LAL + + 4051-6 O104:H2 ο AA + + 4281-7 O104:H-

τ** LAL + + E2348/69 O127:H6 α1 LA + selleck products + Adhesion pattern detected on HeLa cells: localized adherence (LA), localized adherence like (LAL), aggregative adherence (AA) and diffuse adherence (DA) (Vieira et al., 2001). (*) Strains that had eae gene sequenced in this study and (**) strains that carry new intimin subtypes (GenBank accession numbers: 1871-1 (FM872418); 4281-7 (FM872416) and 1632-7 (FM872417). Quantitative assessment of bacterial invasion oxyclozanide was performed with all strains, but different incubation-periods were used to test aEPEC strains (6 h) and tEPEC E2348/69 (3 h), because the latter colonizes more efficiently (establishes the LA pattern in 3 h) than aEPEC strains [3] and induce cell-detachment after 6 h of incubation (not shown). The quantitative gentamicin protection assay confirmed the invasive ability of aEPEC 1551-2 in HeLa cells and showed that 4 of the other 5 aEPEC strains studied were also significantly more invasive than tEPEC E2348/69 (Fig. 1A). The percentages of invasion found varied between 13.3% (SE ± 3.0) and 20.9% (SE ± 2.4), respectively, for aEPEC strains 4051-6 (intimin omicron) and 0621-6 (intimin sigma). When compared to tEPEC E2348/69 (intimin alpha 1) (1.4% ± 0.3), the invasion indexes of all strains were significantly higher (p < 0.05), except for aEPEC strain 4281-7 (intimin tau, 2.4% ± 0.3).

First, they could be followed

for at least 6 months after the initiation of treatment. Second, they had check details proteinuria in excess of 3.5 g/day and serum albumin concentrations of <3.0 g/dl at the start of treatment. Third, MCNS was diagnosed pathologically by light microscopic findings, and confirmed by negative immunofluorescence and typical ultrastructural morphology. Fourth, patients were not treated with corticosteroids or cytotoxic agents. This study was approved by the IRB/Ethics Committee of Yokohama City University Dorsomorphin cell line Medical Center (D-1309006). Therapies and measurements Three groups were included in the present study and were listed in Table 1. Pretreatment baseline parameters, including creatinine clearance, estimated glomerular filtration rate (eGFR), urinary protein excretion, serum total cholesterol concentration, serum albumin concentration, and serum hemoglobin concentration were measured. After discharge, blood pressure, urinary protein excretion, and serum creatinine levels were monitored on an outpatient basis every 2–4 weeks. The adverse effects of cyclosporine and prednisolone were monitored based on medical records. The selectivity index was calculated as the clearance of IgG divided by the clearance of transferrin.

All patients were instructed to follow a low-sodium diet (5 g/day). Patients with marked edema were administered furosemide orally or intravenously, and few patients received intravenous LXH254 albumin. Table 1 Treatment groups Group 1 Patients received cyclosporine (2–3 mg/kg/day) and intravenous methylprednisolone pulse therapy (0.5 or 1.0 g/day Aurora Kinase for 3 days), which were followed by the oral administration of prednisolone (initial doses 30 mg/day). The dose of cyclosporine was maintained at whole-blood trough levels between 50 and 150 ng/ml until the end of the first 6-month

treatment period Group 2 Patients received intravenous methylprednisolone pulse therapy (0.5 or 1.0 g/day for 3 days) followed by the oral administration of prednisolone (initial doses 0.4–0.8 mg/kg/day) Group 3 Patients received oral prednisolone alone (initial doses 0.6–1.0 mg/kg/day) Definitions of remission The response of treatment in nephrotic syndrome was categorized as complete remission, partial remission, or no response. Complete remission was defined as a reduction in proteinuria to below 300 mg/day for three consecutive days. Partial remission was defined as proteinuria of over 300 mg/day, but below 3.5 g/day. No response was defined as proteinuria of more than 3.5 g/day. The relapse of nephrotic syndrome was defined as proteinuria in excess of 1 g/day that lasted for more than three consecutive days during the follow-up.

The obtained fragments ranged from 16 bp to 339 bp (Table  3). Fragments lower than 25 bp were not considered as they did not help in LY294002 order species discrimination and in addition they co-migrate with primers. Time course analysis of restricted samples showed the formation of a band of ~200 bp in several species due to an over-digestion (data not shown) and this invalidated the RFLP profiles. For this reason the protocol has been optimized at 2 hours restriction time. Fragments greater than 360 bp were also not considered due to a possible incomplete digestion of such long fragments.

CB-5083 The obtained gels (Figures  1, 2, 3, 4 and 5) show species-specific profiles for all type-strains other than B. longum and B. thermacidophilum subspecies. This technique does not allow the identification of the subspecies belonging to these species, which displayed identical RFLP profiles. Matsuki et al. [14, 17] proposed specific primers to differentiate the subspecies selleck inhibitor of the species B. longum, while B. thermacidophilum subsp. porcinum and B. thermacidophilum subsp. thermacidophilum can be differentiated according to Zhu et al. [33]. The proposed restriction analysis is efficient in discriminating very closely related species and subspecies as B. catenulatum/B. pseudocatenulatum, B. pseudolongum subsp. pseudolongum/B. pseudolongum subsp. globosum and B. animalis subsp. animalis/B.

animalis. subsp. lactis. Figure 1 Agarose gel electrophoresis of digested hsp60 DNA fragments with HaeIII (negative image). Lane1, ladder 20 bp (Sigma-Aldrich); Lane 2, B. bifidum ATCC 29521; Lane 3, B. asteroides ATCC 25910, Lane 4, B. coryneforme ATCC 25911; Lane 5, B. indicum ATCC 25912; Lane 6, B. thermophilum ATCC 25525; Lane 7, B. boum

ATCC 27917; Lane 8, B. thermacidophilum subsp. porcinum LMG 21689; Lane 9, B. thermacidophilum subsp. thermacidophilum LMG 21395; Lane 10, ladder 20 bp (Sigma-Aldrich). Figure 2 Agarose gel electrophoresis of digested hsp60 DNA fragments with HaeIII (negative image). Lane1, ladder 20 bp (Sigma-Aldrich); Lane 2, B. minimum ATCC 27539; Lane 3, B. pullorum ATCC 27685, Lane 4, B. subtile ATCC 27537; Lane 5, B. gallinarum ATCC 33777; Lane 6, ladder 20 bp (Sigma-Aldrich). Figure 3 Agarose gel electrophoresis of digested hsp60 DNA fragments with HaeIII (negative image). Lane1, ladder 20 bp (Sigma-Aldrich); Lane 2, B. breve ATCC 15700; Lane 3, B. longum subsp. infantis Terminal deoxynucleotidyl transferase ATCC 15697; Lane 4, B. longum subsp. longum ATCC 15707; Lane 5, B. longum subsp. suis ATCC 27533; Lane 6, ladder 20 bp (Sigma-Aldrich). Figure 4 Agarose gel electrophoresis of digested hsp60 DNA fragments with HaeIII (negative image). Lane1, ladder 20 bp (Sigma-Aldrich); Lane 2, B. merycicum ATCC 49391; Lane 3, B. angulatum ATCC 27535, Lane 4, B. pseudocatenulatum ATCC 27919; Lane 5, B. catenulatum ATCC 27539; Lane 6, B. dentium ATCC 27534; Lane 7, B. ruminantium ATCC 49390; Lane 8, B. adolescentis ATCC 15703; Lane 9, ladder 20 bp (Sigma-Aldrich).

Since then many pathological reports demonstrated that the expression of CSE1L in cancer is related to cancer proliferation [6–10], although there

is no experimental studies to show that increased CSE1L expression in cancer cells can enhance the proliferation of cancer cells. CSE1L is highly expressed in cancer; thus, if CSE1L plays Selleckchem CP673451 a role in cancer cell proliferation during cancer development, increased CSE1L expression in cancer cells should be able to increase the proliferation of cancer cells. Our recent study showed that increased CSE1L expression in MCF-7 human breast cancer cells was unable to stimulate cell proliferation [11]. Increased CSE1L expression was also unable to increase the proliferation of other cancer cells including HT-29 human colorectal cancer cells, Hep G2 human hepatocarcinoma cells, 293 kidney cancer cells, and B16-F10 mouse SGC-CBP30 chemical structure melanoma cells (unpublished data). The results of our study further showed that CSE1L enhanced the invasion and metastasis of B16-F10 cancer cells in animal metastasis studies [11]. CSE1L is a cellular apoptosis susceptibility protein and it is highly expressed in various selleck inhibitor cancers; our recent studies showed that CSE1L plays an important role in regulating cancer cell apoptosis induced by chemotherapeutic drugs [12, 13]. Therefore, CSE1L may be a target

for developing strategies to improve the efficacy of cancer chemotherapy as well as for screening more potent anticancer reagents. CSE1L in chemotherapeutic drug-induced cancer cell apoptosis Apoptosis (or programmed cell death) plays an important role in mediating apoptotic stimuli including chemotherapeutic drug-induced

cell cytotoxicity [14]. CSE1L is a cellular apoptosis susceptibility protein, and CSE1L-mediated cancer cell apoptosis was first investigated by Brinkmann et al. using a vector expressing antisense CSE1L cDNA. Their results showed that CSE1L mediated apoptosis induced by Pseudomonas exotoxin, diphtheria toxin, and tumor necrosis factor but did not mediate apoptosis induced by ricin, cycloheximide, staurosporine, or etoposide, a cancer chemotherapeutic drug. Therefore, CSE1L-mediated apoptosis was thought to be limited to selected apoptotic stimuli such as adenosine diphosphate (ADP)-ribosylating Tolmetin toxins and tumor necrosis factor [3, 15]. CSE1L is essential for cell survival, and severe depletion of CSE1L can cause cell death [16]. Those studies used antisense CSE1L cDNA to reduce the cellular CSE1L level; hence the results of their studies might have been a result of those transfected cells expressing not very low levels of CSE1L. Also, they only tested the cancer chemotherapeutic drug, etoposide. An apoptosis-regulating protein should not only regulate apoptosis induced by just ADP-ribosylating toxins and tumor necrosis factor.

8)  Coagulopathy 2 (0.8)  Immunosuppression 2 (0.8)  Leukopenia 0 (0) Primary surgical intervention site, n (%)    Appendix 162 (62.3)  Lower GI tract 51 (19.6)  Upper GI tract 13 (5.0)  Gall-bladder 14 (5.4)  Peritoneal abscess 16 (6.1)  Explorative laparotomy/laparoscopy 4 (1.5) learn more Surgical approach, n (%)    Laparoscopy 135 (51.9)  Laparotomy 116 (44.6)  Percutaneous 9 (3.5) Illness severity markers, n (%)    Parenteral nutrition 52 (20.0)  Central venous catheter 44 (16.9)  Antifungal drugs 28 (10.8)  Enteral nutrition 22 (8.4)

 Invasive mechanical ventilation 20 (7.7)  Immune globulins 0 (0)  Renal replacement therapies 0 (0) ICU transfer, n (%) 24 (9.2) Mean ± SD length of hospital stay, days 10.4 ± 13 Mortality rate, n (%) 6 (2.3) GI, gastrointestinal; ICU, intensive care unit; SD, standard deviation. Figure 1 Antibiotics administered to patients who received monotherapy for first-line treatment of complicated intra-abdominal infections. Cephalosporins included: cefazolin, ceftizoxime, cefotaxime, and Pinometostat nmr ceftriaxone; fluoroquinolones included: ciprofloxacin and levofloxacin; carbapenems included imipenem and meropenem; aminoglycosides included: amikacin, gentamicin and tobramycin. Figure 2 Antibiotic regimens administered to patients who received

combination therapy for the first-line treatment of complicated intra-abdominal infections. Cephalosporins included: cefazolin, ceftizoxime, cefotaxime, and ceftriaxone; fluoroquinolones included: ciprofloxacin and levofloxacin; carbapenems included imipenem and meropenem; aminoglycosides included: amikacin, gentamicin and tobramycin. Other regimens included: aminoglycosides plus ampicillin/sulbactam or piperacillin/tazobactam, or imipenem (n = 4), fluoroquinolones plus amoxicillin/clavulanate, cephalosporins, tygecicline or piperacillin/tazobactam (n = 5), fluoroquinolones plus clindamycin (n = 1). Of the 48 MLN2238 solubility dmso microbiologically evaluable patients (18.4% of the total patient population), 23 (47.9%) intra-operative abdominal site cultures (21 peritoneal swabs, and 2 intra-operative biopsies), 12 (25.0%) abdominal drainage fluid cultures, 11 (22.9%) blood

cultures and 2 (4.2%) surgical wound swabs were performed. Among 34 (70.8%) documented positive cultures, the most frequent isolated pathogen was Escherichia Terminal deoxynucleotidyl transferase coli (58.8%), followed by Klebsiella pneumoniae (14.7%). Due to the low representation of the microbiological evaluable population, antibiotic therapy appropriateness was inferred by covered antimicrobial spectrum and dosing adequacy of starting empiric regimens, as detailed in the methods section. Overall, antibiotic appropriateness rate was 78.8% (n = 205), and was significantly higher in patients receiving combination therapy compared with those treated with monotherapy (97.3% vs. 64.6%). Clinical success chances with appropriate antibiotic therapy were 78.5% (n = 161) and 34.5% (n = 19) with inappropriate therapy. In total, 194 (74.

As shown in Figure 3c, the characteristic peaks of GO (green line) displayed the C=O stretching vibration peak at 1,730 cm-1, the vibration and deformation peaks of O-H groups at 3,428 and 1,415 cm-1, respectively, the C-O (epoxy groups) stretching vibration peak at 1,220 cm-1, and the C-O (alkoxy groups) stretching peak at 1,052 cm-1[25]. After the reaction is conducted for 48 h (red line), the intensities of the FTIR peaks corresponding to the C-O (epoxide groups) stretching vibration peak at 1,220 cm-1 disappeared nearly, the C=O stretching vibration

peak at 1,730 cm-1 decreased dramatically, and the vibration and deformation GW786034 purchase peaks of O-H groups at 3,428 and 1,415 cm-1, respectively, and the C-O (alkoxy groups) stretching peak at 1,052 cm-1 increased slightly. These results further confirmed that some active functionalities ARN-509 concentration (epoxide groups) in GO have been removed. The mechanisms of tailoring GO Since the appearance of GO, the determination of GO structure has been challenging because of its nonstoichiometric chemical composition, which depends on the synthesis method and

the degree of reduction, and the oxygen functional groups in GO have been identified by various kinds of techniques. It is generally agreed that oxygen is present in GO mostly in the form of hydroxyl and epoxide groups on the basal plane, whereas smaller amounts of carboxyl, carbonyl, phenol, lactone, and quinone are present primarily at the sheet edges. The existence of the chemical groups confers new properties on GO such as the perfect monodispersity in water and weak reducibility. Based on the above facts and our experimental results, a probable mechanism is put forward as given in the schematic diagram (Figure 4). Firstly, part of Ag+ ions is preferentially absorbed on the sites of carboxylic groups at the edges of GO by the electrostatic interaction. Then Ag+ ions bonded on GO or freely dispersing in the solution further encounter the reducing groups (e.g., epoxy groups)

on the basal plane of other GO sheets. Thus, Ag+ Arachidonate 15-lipoxygenase ions themselves are reduced to Ag and then generate Ag nanoparticles; meanwhile, the carbon-carbon skeleton is broken which directly leads to the cutting of GO into little pieces. Blasticidin S clinical trial Figure 4 Schematic diagram of tailoring mechanism through solution-phase redox reaction by adding metal ions into solution. Although the feasibility conclusion has been verified through analysis results of UV-vis and FTIR data, we also elaborately investigated the chemical state change of carbon in GO by XPS technology. Figure 5a shows the C1s XPS of GO sheets. There are four different peaks detected that centered at 284.5, 288.4, 293.8, and 296.6 eV, corresponding to C=C/C-C in aromatic rings, C-O (epoxide and alkoxy), C=O, and COOH groups, respectively [26]. After adding Ag+ ions into solution for 48 h, the distinct changes of C1s XPS are detected in Figure 5b.

According to the symmetry, the y-direction

component of electric field E D (r A ) also vanishes, as shown in Figure 2e. Therefore, only the x-direction components of the electric fields contribute to the RET rates; for different θ A values, we have (2) Figure 2 Energy transfer between donor see more and acceptor with different dipole moment directions in single square nanorod. (a) Schematic picture on xy plane. (b) Schematic picture on xz plane. (c) The nETR with a = 40 nm, d = 20 nm, L = 250 nm, and different values of θ D and θ A . The schematic pictures for the electric field at the position of the acceptor induced by the donor with θ D = 0° (d) in vacuum and (e) in the nanorod structure. It is thus straightforward to get (3) resulting in the same nETR shown in Figure 2c. While for the case of θ D = 60° and θ A = 60°, it can be seen that the nETR decreases evidently, the resonance wavelength is about 1,157 nm, and the maximum enhancement is reduced to about 7,500. The above results demonstrate that, in order to produce

high RET enhancement in the single nanorod structure, the direction of the donor or acceptor dipole should be along the principle axis of the nanorod, otherwise the enhancement decreases evidently. In practical devices, it is very difficult to satisfy the parallel condition between the dipole moments of the donor and acceptor. In order to improve the RET rate for donor-acceptor pairs with nonparallel MS-275 price dipole moments, according to the above results, we propose new V-shaped structures. Figure 3a is the schematic picture of a V-shaped structure; the angle between the principle axis of each nanorod branch and the connection line of the dipoles are denoted as θ 1 and θ 2, respectively. For the dipole directions θ D = 60° and θ A = 60°, we also choose θ 1 = 60° and θ 2 = 60°, so the principle axis of each nanorod branch in this structure is aligned

to a dipole. The distance from each dipole to the end of the nanorod is d = 20 nm. The height and width Thiamine-diphosphate kinase of each nanorod are set to be a = 40 nm. In order to improve the coupling between these two nanorods, we introduce a sharp corner part with gap widths g from the other ends of the nanorods. Figure 4a displays the nETR spectra for V-shaped structures shown in Figure 3a with different gap widths g, for L′ = 290 nm, compared with the case of single nanorod. It can be seen that the nETR BIBW2992 cell line spectrum can be modulated by controlling the gap widths g. When the gap widths decrease, the resonance wavelength is red shifted, and the maximum enhancement increases. When g = 0 nm, the structure becomes whole, and the main resonance wavelength is remarkably red shifted and exceeds 1,800 nm. We can thus design the V-shaped structure with proper gap widths to obtain a nETR spectrum with approximately the same resonance wavelength as that in the single nanorod.

9 x105 A1 – I/ATT 3 – 93 (ATT)/4 (ATA) NN018 BMS202 manufacturer chronic LAM 36 4.6 x103 A1 – V/GTG 6 94 (GTG) – NN019 chronic LAM 36 3.0 x103 A1 M/ATG – 96

– 4 (ATA) NN027 chronic LAM 36 2.8 x104 A1 M/ATG – 95 – 5 (ATT) NN037 chronic LAM 36 4.8 x105 A1 M/ATG – 100 – - NN079 chronic LAM 36 9.6 x103 A1 M/ATG – 100 – - NN087 chronic LAM 72 1.1 x104 A1 M/ATG – 100 – - NN007 chronic LAM 84 2.8 x104 A1 – V/GTG – 100 (GTG) – NN028 chronic LAM 108 1.8 x109 A1 V/GTG – 100 (GTG) –   NN032 chronic LAM + TDF 132 1.2 x104 A1 – V/GTG – 100 (GTG) – NN025 chronic LAM 05 4.3 x104 A2 M/ATG – 100 – - NN014 chronic LAM 07 1.4 BI 10773 purchase x105 A2 – I/ATT – - 100 (ATT) NN042 chronic LAM 12 5.4 x107 A2 – V/GTG 6 94 (GTG) – NN022 chronic LAM + ADV 24 1.7 x105 B – I/ATT – 25 (GTG) 70 (ATT) NN074 chronic LAM 06 6.5 x105 D2 – V/GTG – 100 (GTG) – NN125 chronic LAM + TDF 12 2.5 x103 D2 – I/ATT – - 100 (ATT) NN001 chronic LAM 60 2.4×104 D3 – V/GTG – 100 (GTG) – NN091 chronic LAM 06 4.3 x103 D3 – I/ATT – - 100 (ATT) NN096 chronic LAM 06 3.1 x103 D3 M/ATG – 100 – - NN097 chronic LAM 06 5.3 x106 D3 M/ATG – 95 – 5 (ATT) NN129 chronic LAM 06 7.2 x108 D3 – V/GTG – 95 (GTG) 5 (ATT) NN029 chronic LAM 12 7.0 x104 D3 M/ATG – 86 4 (GTG) 6 (ATA)/4 (ATT) NN038 chronic LAM + TDF 12 2.9 x105 D3 M/ATG – 100 – - NN077 chronic LAM 12 9.7 x105 D3 – I/ATT 4 – 96

(ATT) NN034 chronic LAM + ADV 24 1.0 x105 D3 – V/GTG – 90 (GTG) 10 (ATT) NN075 AZD3965 datasheet chronic LAM 60 3.2 x103 D3 M/ATG – 100 – - NN031 chronic LAM 72 6.8 x107 D3 – V/GTG – 100 (GTG) – NN126 chronic LAM 06 1.9 x108 F1b – I/ATC – 30 (GTG) 70 (ATC) NN105 chronic LAM 06 3.7

x108 F2 – V/GTG – 100 (GTG) – NN078 chronic LAM 12 1.2 x106 F2 M/ATG – 95 – 5 (ATT) NN134 chronic LAM 12 2.7 x104 F2 – I/ATT – 25 (GTG) 75 (ATT) NN020 chronic LAM 48 3.7 x104 F2 M/ATG – 100 – - Surprisingly, acute HBV patients had relatively low HBV titers compared to what would have been expected for an acute HBV infection, ranging from 6.2 x 102 to 1.4 x 106 copies/mL (mean viral load, 2.0 x 105 copies/mL; median viral load, 2.0 x 104 copies/mL). The mean viral load was 1.4 x 105 copies/mL, and the median was 5.6 x 104 copies/mL. The direct PCR Sanger sequencing method (population-based sequencing approach) detected only the major population in our assays. Literature reports indicate that only minor populations present as more MRIP than 20% of the total quasispecies pool can be detected by the Sanger method [26]. To test the ability of pyrosequencing to detect minor sequence variants of the YMDD population, we evaluated different proportions of plasmids containing WT (rtM204) and MUT (rtV204) sequences.