p.) twice weekly for a total of 9 doses (Figure 2A and B). Compared with controls, bevacizumab at all 3 doses significantly inhibited tumor growth in both SCC1 (p values of 0.04, 0.05, and 0.03, respectively) and H226 groups (p values of 0.06, 0.04, and 0.01). There was no significant Capmatinib purchase statistical difference

in anti-tumor activity observed among the three bevacizumab groups. This result is consistent with other reports demonstrating the maximal inhibitory activity of bevacizumab in tumor xenograft models at approximately 1–2 mg/kg [6]. Based on this result, a dose of 0.75-1 mg/kg of bevacizumab was chosen for subsequent experiments to investigate the combination of bevacizumab and radiation. Figure 2 Inhibitory effect of bevacizumab on tumor growth in SCC1 (A) and H226 (B) xenograft models. Four groups of

mice (n = 3 tumors per treatment group for each cell line) were treated with: IgG (control), bevacizumab 1 mg/kg, 5 mg/kg and 25 mg/kg. Bev, bevacizumab. Bevacizumab selleckchem inhibits the formation of HUVEC capillary-like network In the tube formation assay, we observed a quick attachment of HUVEC onto the matrigel in the control wells. Indeed, cells mobilized on the gel, spread out and generated lateral processes to form intercellular connections within 3 hours of seeding, with a network of endotubes well established by 6 hours. This capillary-like network was well maintained after 22 hours in the control wells (Figure 3A). In the 0.5 μM bevacizumab wells, little inhibitory effect was observed (Figure 3B). However, bevacizumab at 5 μM clearly prevented the mobilization and generation of lateral processes of HUVECs with

only fragmented tubes being seen (Figure 3C). As seen in the figures, the total numbers of intact endotubes in the control, bevacizumab 0.5 μM and bevacizumab 5 μM groups at 22 hours of incubation are 42, 39, and 0, respectively. This result suggests that bevacizumab inhibits not only HUVEC growth but also endothelial cell function. Figure 3 Inhibitory effect of bevacizumab on HUVEC capillary-like network formation following Carnitine palmitoyltransferase II 22 hours of treatment: (A) IgG (control), (B) Bevacizumab 0.5 μM, and (C) Bevacizumab 5 μM. Bevacizumab enhanced radiation-induced apoptosis in HUVEC To investigate the apoptotic effect of radiation and bevacizumab, we treated HUVEC with bevacizumab, radiation, or both (Figure 4). Apoptosis was observed in cells treated with radiation alone and combined radiation and bevacizumab, but not in the control or bevacizumab alone group. PU-H71 cell line Moreover, this experiment demonstrated the ability of bevacizumab to enhance radiation-induced apoptosis in HUVEC, with 5.1% and 9.9% of cells treated with combined therapy undergoing apoptosis after 24 and 48 hours respectively versus 2.1% and 3.2% in cells treated with radiation alone. Figure 4 Effect of bevacizumab with and without radiation on HUVEC apoptosis.

The region of C-prM gene junction was selected for serotyping as the region is not very hyper variable and most of the mutations reported are of silent type [12]. Lifecycle HKI-272 mw of dengue virus involves both human and mosquitoes and this might be the reason for low rate of variation among dengue virus as compared to other RNA viruses. According to several reports, the classification of dengue genotypes is based on less than 6% of nucleotide

divergence within a selected genomic region [12, 28]. Dendrograms were drawn to study the evolutionary history of the sequenced serotypes as well as their genotypes which showed that serotype 2 circulating in 2007-2009 belonged to genotype IV. Strains from Northern India, China and Indonesia also fall in this subtype [12]. No particular pattern of genotype distribution can be inferred for serotype 2 as different genotypes spread in diverse locations. Raf inhibitor For serotype 3, only sequences of capsid region from genotype I and III are reported. So the tree was created using global sequences of genotype I and III only. However, the tree visibly shows that the studied serotype 3 has genotype III. It is clear from the findings of our study that there is no definite pattern of distribution of subtype III of dengue virus 3 worldwide [4]. The previously sequenced three strains from Karachi (Pakistan)

in 2005 [20] also have same genotype emphasizing the fact that genotype III of dengue virus 3 prevails in Pakistan. There is not much data available from Pakistan on serotypes of dengue virus; this study is the first one to characterize serotypes 2 and 3 in their respective subtypes. The only limitation of this study is small number of sequenced samples. There is a need for more randomized and multi-analysis studies to be conducted on serotyping and subtyping of different dengue strains in Pakistan; in this way a

clearer view on spread of dengue virus can be made. Conclusions Based on the findings of the current study we conclude that the predominant serotypes Parvulin of dengue virus circulating in Pakistan are 2 and 3. Ample number of cases with mixed serotypes (serotype 2 and 3) are seen and might be common in all regions of this country. The major genotypes circulated in the study period are subtype IV of dengue virus 2 and subtype III of dengue virus 3. check details Methods Patients Samples and Extraction of viral RNA A total of 114 serum samples were received from Gurki Trust hospital Lahore and Sheikh Zayed Medical Complex Lahore. Viral RNA was extracted from 140 μl of serum sample using Nucleospin Viral RNA Extraction Kit (Macherey-Nagel, Germany) with slight modifications. Briefly, 600 μl of lysis buffer was added to 140 μl of serum sample and vortexed for few seconds. Then the samples were incubated at 70°C for 5 minutes. Then 600 μl of absolute alcohol was added. The sample was loaded in the column tube and centrifuged at 13000 rpm for one minute. A 500 μl of buffer RAW was added and centrifuged at 13000 rpm for 5 minutes.

Also, SiNWs are regarded to be a good candidate for efficient thermoelectric devices. Experimentally, thermal conductivities of SiNWs with diameters ranging from 22 to 115 nm [1] and from about 15 to 50 nm [2] have recently been measured and showed unusually low thermal transport properties. The measured thermal conductivities show different temperature dependence for different diameters of nanowires due to the confinement effects to nanometer

size. To understand the thermal transport properties of SiNWs less than 100 nm in diameter, we need to BTSA1 datasheet consider the phonon problems from an atomistic point of view. Theoretically, Mingo et al. [3] calculated thermal conductivities of SiNWs with diameters larger than 35 nm, using the phonon dispersion relation from the data of bulk silicon, and showed good agreement with the experiments. This shows that thermal

conductance Selleckchem I-BET151 calculations with the Boltzmann VX-680 solubility dmso transport formula or molecular dynamics calculations are effective at high temperature in diffusive regime. However, for phonon transport at low temperature or with diameters less than 30 nm, the effects of nanometer-scale structures such as confinement and low speed modes on phonon transport become significant [3]. For such regimes, we need the computational approach, taking the quantum effects explicitly into account. These effects for thermal transport can be included when we use the transmission approach, where the Landauer formula [4] or the non-equilibrium Green’s function (NEGF) technique based on the Keldysh’s theory has been widely studied [5]. The NEGF approach has been well established [6, 7] for electron transport and also the formulation is derived for phonon transport [8]. Recently, some theoretical works have been performed based on the atomistic models using the NEGF technique to calculate the thermal conductances of SiNWs [9–11] and carbon nanotubes [12]. In the present work, we treat the thermal conductance of SiNWs in comparison to the diamond nanowires (DNWs) which have the same DCLK1 atomistic configurations but are made

of the different atomic types. Since the bulk diamond has very high thermal conductivity, we expect that DNWs might also have high thermal conductivity. Here we use the NEGF technique with empirical Tersoff-Brenner interatomic potentials for the atomistic calculations of thermal conductance of SiNWs and DNWs. We present thermal conductance of SiNWs with diameters from 1 to 5 nm with and without vacancy defects and DNWs with diameters ranging from 1 to 4 nm without defects. The diameter dependences of thermal conductances of SiNWs and DNWs with no defects are presented for the temperature ranging from 0 to 300 K. We show how the thermal conductances of SiNWs and DNWs change their behaviors as the temperature decreases with their thickness.

001   Yes 105 63.8     No 132 43.2    Employment status at discharge     <0.001   Employed 185 60     Unemployed 41 12.2    Patient wish for return to work     <0.001   Want 170 61.2     Do not want 35 22.9    Family wish for patient return to work     0.199   Want 131 58.8     Do not want 17 41.2    Satisfaction with social participation     <0.001   Yes 82 59.9     No 55 55    Collaboration with industrial physicians     0.062   Yes 23 78.3     No 108 56.5    Cooperation of workplace supervisors     0.016   Yes 50 78     No 61 55.7    Coordination of the work environment     1   Yes 10 70     No 94 71.3    Cooperation with vocational rehabilitation     0.41   Yes 17 76.5     No 97 62.9    Support of

medical institutions on return to work     0.001   Yes 43 74.4     No 131 45.8   NCT-501 cell line Total number of patients does not always equal 250 because of missing data Score 0 no symptoms, Score 1 no significant disability despite symptoms, Score 2 slight disability, Score 3 moderate disability,

Score 4 moderately severe disability, and Score 5 severe disability * mRS—Rankin scale Fig. 1 Proportion of patients returning to work during the 18 months after stroke onset After adjustment for age, gender, and BI at initial rehabilitation, the following variables showed significant associations with the return to work at 18-month follow-up: job type, work position, etiological diagnosis, upper extremity function, walking ability, spasticity, TSA HDAC manufacturer visuospatial neglect, aphasia, attention dysfunction, memory dysfunction, and intelligence dysfunction. Since etiological diagnosis and work position violated proportional hazard assumption in visual diagnosis with Kaplan–Meier curves, we excluded these variables in further analysis, leaving nine variables for further multivariable find more analysis (Table 2). Table 2 Selected candidate variables associated aminophylline with return to work within 18 months of onset after adjusting for

age, gender, and Barthel index at initial rehabilitation Variables Reference Hazard ratio 95 % confidence interval Job type White collar versus blue collar 1.6 1.1–2.2 Upper extremity function Normal or mild versus severe 3.6 1.8–7.4 Moderate versus severe 2.5 1.1–5.6 Walking ability Independent versus dependent 4.8 2.2–10.6 Spasticity No versus yes 2.9 1.3–6.3 Visuospatial neglect No versus yes 4.7 1.7–12.9 Aphasia No versus yes 3.3 1.7–6.3 Attention dysfunction No versus yes 3.1 1.6–6.0 Memory dysfunction No versus yes 2.8 1.4–5.6 Intelligence dysfunction No versus yes 2.2 1.1–4.4 In stepwise Cox proportional hazard regression analysis, with adjustment for age, gender, and BI at initial rehabilitation, significant predictors of return to work at 18-month follow-up after stroke were job type, aphasia, attention dysfunction, and walking ability (Table 3). Specifically, those who had independent walking ability, were engaged in white-collar jobs, and were without aphasia and attention dysfunction were significantly more likely to return to work.

Invasion of P. gingivalis into gingival epithelial cells induces the nucleation of actin filaments to form microspike-like protrusions and long stable microfilaments distributed throughout the cells [15]. Cytoskeletal reorganization may facilitate phagocytic cup formation and subsequent bacterial engulfment. Cytoskeletal remodeling resulting from bacterial internalization can spatially redistribute enzymes such as MAPK family members and their substrates, and thus influence intracellular signaling pathways [16, 17]. P. gingivalis invasion of human gingival epithelial cells causes activation of JNK (c-Jun N-terminal see more kinase) and down-regulation of ERK1/2 (extracellular

signal regulated kinase), whereas Foretinib molecular weight p38 and NF-κB (Nuclear factor-Kappa click here B) are not affected [18]. After invading gingival cells, P. gingivalis ultimately localizes to the perinuclear region [2, 4]. Despite the burden of a large number of intracellular P. gingivalis, both gingival epithelial cells and fibroblasts demonstrate an initially decreased but later increased rate of apoptosis upon bacterial challenge [19–22]. Presumably, this temporal shift from cell survival to apoptosis is utilized by P. gingivalis to reach an initial intracellular concentration

while escaping host immune surveillance, and a later dismantling of host cells to facilitate disease transmission. This paper reports results from experiments using an in vitro model of P. gingivalis−osteoblast interactions. The findings suggest that P. gingivalis uses its major fimbriae to bind to integrin α5β1 on osteoblasts and reorganize actin microfilaments to invade osteoblasts. In addition, infected osteoblasts demonstrate activation of the JNK pathway, as well as an initial

increase in cellular survival with a subsequent increased cellular death, as reported for other periodontal cells. Methods Osteoblast isolation Primary mouse calvarial osteoblasts were isolated from 7-day-old CD-1 mice using the method described by Wong and Cohn [23]. Briefly, calvaria were subjected to four sequential 15-minute digestions in an enzyme mixture containing Autophagy activator 0.05% trypsin and 0.1% collagenase P at 37°C. Cell fractions 2–4 were pooled and resuspended in Dulbecco’s Modified Eagle’s Medium (DMEM) containing 10% fetal bovine serum (FBS), 100 U/ml penicillin and 100 μg/ml streptomycin, then filtered through a 70 μm cell strainer. Cells were plated at a density of 1 × 104 cells/cm2 and the medium was changed 24 h later. All animal-related experiments were approved by the Center for Laboratory Animal Medicine and Care at the University of Texas Health Science Center at Houston (approved animal protocol number HSC-AWC-10–145). Bacteria and culture conditions Porphyromonas gingivalis strain ATCC 33277 was grown anaerobically at 37°C in a Coy anaerobic chamber under an atmosphere of 86% nitrogen, 10% carbon dioxide, 4% hydrogen.

(OD = 30 in Figure 1). Altogether, the results presented in Figure 3 underline

the presence of at least one substance in the extract that restricts PM production, enhances growth at lower levels, and retards growth at higher levels. To check if accumulated bacteriochlorophyll a precursors influence the PM synthesis by the cells, PPIX (chemically synthesized) learn more and Mg-PPIX-mme (isolated from microaerobic HCD cultures supernatants) were added to a growing culture at OD = 1, the point at which PM synthesis is https://www.selleckchem.com/products/pf-04929113.html normally induced by oxygen depletion. Tetrapyrole precursors were supplemented in amounts equivalent to those observed under HCD conditions. Addition of either PPIX or Mg-PPIX-mme resulted in slightly lower PM levels compared to the control (MeOH) (see Additional file 1: Figure S1). However, the reduction was weaker than the effect caused by the addition of the culture extract

or by resuspending fresh cells in culture supernatant. R. rubrum produces different types of bioactive AHLs To check the R. rubrum cultures for bioactive AHL, sterile-filtered culture supernatant from a Fed-Batch HCD culture was analyzed with a thin layer chromatography bioassay with Agrobacterium tumefaciens NTL4 as an indicator strain [18]. These assays clearly demonstrated the bioactivity of R. rubrum HCD culture extracts with the TraR-dependent quorum sensing system of A. tumefaciens NTL4, indicated by intense blue spots on the agar-overlaid TLC plates 3-Methyladenine mouse (see Additional file 1: Figure S2). The extracts were further examined by HPLC-MS for the presence of AHLs. For identification AZD9291 research buy and quantification of HPLC peaks, a commercially available C8oxo-HSL and a derived C8OH-HSL (see Material and Methods) were employed as standards for comparison of retention time, MS signals and DAD spectral properties. In the reversed phase HPLC-separated extract, the following six AHLs could be identified in the supernatant of R. rubrum HCD cultures: N-(3-hydroxhexanoyl)-homoserine lactone (C6OH-HSL), N-(3-hydroxyoctanoyl)-homoserine lactone (C8OH-HSL), N-(3-octanoyl)-homoserine

lactone (C8-HSL), N-(3-decanoyl)-homoserine lactone (C10-HSL), N-(3-hydroxydecanoyl)-homoserine lactone (C10OH-HSL) and N-(3-hydroxydodecanoyl)-homoserine lactone (C12OH-HSL) (for m/z values, see Additional file 1: Table S3). The concentration of C8OH-HSL in the supernatant of an aerobic Fed-Batch cultivation at OD = 50 was ~330 μM. The concentrations of the other AHLs were not determined due to the lack of a reference standard. Since only very small peaks of C10-HSL and C12OH-HSL were detected, these compounds were not considered further. The more abundant peaks were isolated by semi-preparative HPLC as pure fractions and applied to the A. tumefaciens NTL4 autoinducer bioassay on agar plates (Figure 4). C6OH-HSL, C8-HSL, C8OH-HSL, and C10OH-HSL caused a blue colour response of the indicator strain thus confirming the results obtained with crude dichloromethane extracts.

01). Another HIF-1α binding site, located at -166 bp~-163 bp of the survivin

core promoter, was also mutated, but there was no BIBW2992 purchase relative difference in transcriptional activity between the normal and mutated binding site promoter constructs. Figure 3 Site directed mutagenesis of the HIF-1α binding site on the survivin promoter decreases transcription activity of the survivin promoter. A: Nucleotide sequence of the survivin promoter. The putative binding sites for transcription factor are boxed. The GTGC sequence in -19 ~ -16 bp of survivin promoter was changed to AGC BMS202 in vitro by mutation. B: A549 cells were transfected with pGL3-Basic without promoter (negative control), pGL3-SVP-229-luc (mutant plasmid), and pGL3-SVP-230-luc (normal plasmid). The relative activity of survivin promoter

was analyzed by luciferase assay. The graph shows the statistical results. Data are given as means ± SD, n = 3, ** p < 0.01. Decreased HIF-1α expression leads to decreased survivin expression in A549 cells A549 cells were treated with dsRNA (siRNA) targeted to HIF-1α mRNA and the expression levels of HIF-1α and survivin mRNA, and protein in were detected. As shown in Fig. 4, the mRNA and protein expression levels of HIF-1α and survivin in A549 cells significantly decreased after the treatment with HIF-1α siRNA as compared with negative control siRNA ASP2215 purchase and untreated controls (p < 0.05). Figure 4 Decreased HIF-1α expression leads to decreased survivin expression

in A549 cells. Cells were cultured in 10% FBS medium overnight, Lck followed by treatment with HIF-1α-siRNA for 48 h. Total RNAs were isolated and analyzed by quantitative, real time, reverse transcription-PCR to determine the changes of survivin (A) and HIF-1α (B) mRNA. The relative levels of survivin and HIF-1α mRNA are expressed as a ratio of the amount of survivin (A) or HIF-1α (B) PCR products to the amount of GAPDH PCR product. C: The expression of survivin and HIF-1α protein in A549 cells following HIF-1α-siRNA treatment as detected by Western blot analysis. The relative expression levels of HIF-1α (D) and survivin (E) protein is expressed as a ratio of the amount of survivin or HIF-1α protein to the amount of β-actin protein. Data are given as means ± SD, n = 3, ** p < 0.01. Data are given as means ± SD, n = 3, ** p < 0.01. Discussion Apoptosis has negatively regulates the occurrence and development of tumors and prevents the rapid growth of tumor cells. Apoptosis is co-regulated by apoptosis-promoting factor and apoptosis-inhibiting factors (such as members of the IAP family of proteins) [22, 23]. Survivin, the smallest protein of IAP family, is rarely expressed in differentiated tissues and highly express in 75 ~ 96% of tumor tissues [4]. In this study, we found that survivin was expressed in 81.6% of NSCLC tissues, and not expressed in tissues from patients with benign lung diseases.

Imaging also revealed the presence of a ruptured abdominal mass (Figure  3). The exploratory laparotomy discovered 3000 ml of blood in the abdominal cavity. The liver was non-cirrhotic, and there was an actively bleeding invasive tumor in the left lateral triangular ligament of the liver. The tumor was resected with an appropriate margin and the specimen was histologically confirmed as a 5-cm HCC with negative margin. The post-operative

course was https://www.selleckchem.com/products/psi-7977-gs-7977.html unremarkable, and the patient was discharged on the 10th day post-surgery. Figure 1 A contrast extravasation is shown from a mass like lesion on the lateral border of the liver (arrow) and hemoperitoneum. Figure 2 Abdominal CT showes diaphragm invasion of the mass like lesion (arrow). Figure 3 VX-765 price A liver surrounded by a large volume of fluid

is seen. An approximately 4cm sized low density lesion is located in the periphery of the lateral segment (arrow). Discussion HCC is the most common primary malignant tumor of the liver [1, 2]. Lai and W. Y. Lau analyzed literature published between 1970 and 2004 and found 1500 published cases of spontaneous HCC rupture [2]. This complication is observed in 3% of the Western population and in 14% of the Asian population, and mortality ranges between 25 and 75% [2, 11]. The click here mechanism behind the spontaneous rupture of HCC remains unclear but a number of hypotheses to explain this phenomenon have been published. Possible etiological factors include subcapsular location, tumor dimensions, portal hypertension, tumor necrosis, local increase in venous pressure due to outflow reduction caused by neoplastic invasion, and previous vascular injury which might predispose a patient to HCC rupture and to the rupture of smaller lesions in other locations [12, 13]. Usually, the initial symptom is

sudden epigastric or right hypochondrial pain. Some patients present with shock, and most have signs of peritonitis, abdominal distension or both. Patients also often present paracentesis-positive with blood-stained ascites [14]. In the SSR128129E presented case, the patient complained of acute abdominal pain and distension. Preoperative diagnosis of HCC rupture is difficult in patients with no previous history of cirrhosis or HCC. Vergara et al. reported that an accurate preoperative diagnosis of ruptured HCC was predicted in only 25% of cases, despite shock being present in 33 – 90% of the patients [15]. Doppler ultrasound and CT imaging are useful in delineating hemoperitoneum and liver tumors and CT is specifically useful in detecting HCC rupture by visualizing the tumor and blood loss. The peripheral location and protrusion of the tumor and discontinuity of the hepatic surface and surrounding hematoma with high attenuation on CT are very helpful signs in the diagnosis of ruptured HCC [16].

reichenowi (HBs 5, 14, 36, 64, 54, 60, 79, 210, 88, 131, 153, 171, 163, and 260, in order of frequency in the P. reichenowi genome). this website sequence homology among such distantly related parasites reflects the ancient origin of var genes, and the strong balancing selection that maintains these sequence variants through millions of years of evolution [28]. The genomic var dataset, comprising 1851 sequences, contained 1708 unique sequences by amino acid identity (aa-types), with an average of

Saracatinib purchase 34.92 aa-types per isolate. There were 2–10 HBs per DBLα tag (Figure  1), and the genomic dataset contained 28 unique HBs in 398 unique combinations (398 HB-types), with an average of 5.19 HB-types per isolate. The cDNA dataset PF299 order for all 250 isolates, comprising 4538 sequences, contained 3925 unique sequences by amino acid identity, with an average of 18.15 aa-types per isolate. These sequences contained 29 HBs in 557 unique combinations, with an average of 2.23 HB-types per isolate. Figure 1 The homology block architecture of DBLα

tags. (A) The architecture of a var gene and the PfEMP1 protein it encodes. The number, identity and order of the DBL and CIDR domains varies. One of the only constants is the presence of a single DBLα domain, which is located at the N-terminal end of the coding region. The DBLα domain is made up of subdomains S1-3. The tag comes from a region of S2. Twenty-nine distinct homology blocks were found within the cDNA dataset and almost the same set (all but HB 556) were found within the genomic dataset. (B) The output from Vardom Server [8] with added HB labels for the dominantly expressed sequence

tags for four of the highest rosetting isolates within the cDNA dataset, chosen as follows: from the symptomatic second isolates with the highest rosetting rates (i.e., the 22 isolates with transformed rosetting rates over 0.5), we identified those with a single dominantly expressed sequence (i.e., approximately twice as large as the expression rate of any other sequence or more, and larger than the rest of the sequences’ expression rates combined), and this amounted to seven sequences; the four shown are those with good HB coverage (more than 3 HBs within the tag). It is indicated whether the patient from which the sample was taken exhibited impaired consciousness (IC). For the dataset of cDNA var tags for all 250 isolates, the average fraction of the sequence that is missed by HB alignment is 12.7% (when the sites before the start of the first HB and after the end of the final HB are excluded). The frequency of the HBs varied, with only a few at intermediate frequencies (Figure  2A). The sequences were highly variable in their HB composition (Figure  2B), and reflected the previously described recombining groups (Figure  2C).

An optimal cutoff point of 77 mP is indicated (arrow). AUCROC = 0.959 (95% confidence interval = 0.908 to 0.986). FP assay can be used in the study of antigen-antibody interaction, and the attachment of fluorescein to antigen does not affect its ability to bind with an antibody. The only limitation of the FP assay is the size of the antigen, and the principle of FP assay restricts that only the micromolecular antigen is

suitable for interaction analysis. The more differences of molecular weight between antigen and antibody exist, the more differences of FP values between free antigen and antigen-antibody complex can be measured. The molecular mass of synthetic antigenic this website peptides is far smaller than general antigens, so they are suitable for the screening of antigenic epitopes by the FP method. By investigating the interaction between peptide and standard antibody sample, the antigenicity of this https://www.selleckchem.com/products/BIRB-796-(Doramapimod).html peptide can be easily determined. For instance, when the QD-labeled peptides are mixed with the Selleck PLX 4720 standard antibody in solution, if the peptides have antigenicity, they can bind with antibodies rapidly. The formations of antigen-antibody complex slow the rotation of the fluorescent tracer and thereby increase the polarization of the emitted light compared with only peptides existing in solution. On the other hand, the polarization has no change if the peptides have no antigenicity. In

other words, a high FP value SPTLC1 represents a strong antigenicity of peptides, and a low value represents a weak antigenicity of peptides after FP measure. When the peptides reacted with standard antibody-positive serum, in this report,

the measured FP values of the 10 of 11 HBV synthetic peptides were between 200 and 250 mP, far higher than the FP values of the peptides that reacted with the standard antibody-negative serum, which were only about 150 to 170 mP, and these peptides may have antigenicity. In order to optimize the FP assay used in detecting the interaction of antigenic peptide and antibody, we investigated the effects of different concentrations of fluorophore-labeled peptides, different dilution times of serum samples, and different incubation times of antigen-antibody mixture on FP assay. The obtained optimal factors are as follows: 1 nmol/L of fluorophore-labeled peptides, 1:25 of dilution times of serum samples, and 15 min of incubation time of antigen-antibody mixture. The established FP assay not only can be used to identify the antigenicity of peptides with standard antibody, but can also be used to detect antibodies in serum samples with known antigenic peptides because the usages of FP assay in the two aspects share the same principle and procedures. By analyzing the antibody levels against 10 antigenic peptides in 159 anti-HBV surface antigen-positive antiserum using FP assay, we found that the antibody levels against nos.