J Clin Microbiol 1985, 21:585–587.PubMed 27. Ralph D, McClelland M, Welsh J, Baranton G, Perolat P: Leptospira species categorized by arbitrarily primed polymerase chain reaction (PCR) and by mapped restriction polymorphisms in PCR-amplified rRNA genes.

Journal of #https://www.selleckchem.com/products/i-bet151-gsk1210151a.html randurls[1|1|,|CHEM1|]# bacteriology 1993, 175:973–981.PubMed 28. de la Pena-Moctezuma A, Bulach DM, Kalambaheti T, Adler B: Comparative analysis of the LPS biosynthetic loci of the genetic subtypes of serovar Hardjo: Leptospira interrogans subtype Hardjoprajitno and Leptospira borgpetersenii subtype Hardjobovis. FEMS Microbiol Lett 1999, 177:319–326.PubMedCrossRef 29. de la Pena-Moctezuma A, Bulach DM, Adler B: Genetic differences among the LPS biosynthetic loci of serovars of Leptospira interrogans and Leptospira borgpetersenii. FEMS Immunol Med Microbiol 2001, 31:73–81.PubMedCrossRef 30. He P, Sheng YY, Shi YZ, Jiang XG, Qin JH, Zhang ZM, Zhao GP, Guo XK: Genetic diversity among major endemic strains of Leptospira interrogans in China. BMC genomics 2007, 8:204.PubMedCrossRef 31. Yan J, Dai BM, Yu ES, Qin JC, Guo XK, Jiang XG, Mao YF: Leptospirosis. 3rd edition. People’s Medical Publishing House; 2005:183–186. 32. ACP-196 clinical trial Gu JW,

Jiang XG, Guo XK: Servor and Alternation of Leptospira in China. Chinese Journal of Practice Medicine 2005, 4:22–23. 33. Ren SX, Fu G, Jiang XG, Zeng R, Miao YG, Xu H, Zhang YX, Xiong H, Lu G, Lu LF, Jiang HQ, Jia J, Tu YF, Jiang JX, Gu WY, Zhang YQ, Cai Z, Sheng HH, Yin HF, Zhang Y, Zhu GF, Wan M, Huang

HL, Qian Z, Wang SY, Ma W, Yao ZJ, Shen Y, Qiang BQ, Xia QC, Guo XK, Danchin A, Saint Girons I, Somerville RL, Wen YM, Shi MH, Chen Z, Xu JG, Zhao GP: Unique physiological and pathogenic features of Leptospira interrogans revealed by whole-genome sequencing. Nature 2003, 422:888–893.PubMedCrossRef 34. Wangroongsarb P, Chanket T, Gunlabun K, Long do H, Satheanmethakul P, Jetanadee S, Thaipadungpanit J, Wuthiekanun V, Peacock SJ, Blacksell SD, Smythe LD, Bulach DM, Kalambaheti T: Molecular typing of Leptospira spp. based on putative O-antigen polymerase gene (wzy), the benefit over 16S rRNA gene sequence. FEMS Microbiol Leukotriene-A4 hydrolase Lett 2007, 271:170–179.PubMedCrossRef 35. Ellinghausen HC Jr, McCullough WG: Nutrition of Leptospira Pomona and Growth of 13 Other Serotypes: Fractionation of Oleic Albumin Complex and a Medium of Bovine Albumin and Polysorbate 80. American journal of veterinary research 1965, 26:45–51.PubMed 36. Cole JR Jr, Sulzer CR, Pursell AR: Improved microtechnique for the leptospiral microscopic agglutination test. Applied microbiology 1973, 25:976–980.PubMed 37. Bajani MD, Ashford DA, Bragg SL, Woods CW, Aye T, Spiegel RA, Plikaytis BD, Perkins BA, Phelan M, Levett PN, Weyant RS: Evaluation of four commercially available rapid serologic tests for diagnosis of leptospirosis.

The device size is 4 × 4 μm2. Every cycle data was captured during measurement. The P/E voltages were +2/−2.2 V. Both HRS and LRS were read out at +0.1 V, and pulse width was 500 μs. The P/E cycles are not stable as we expected. Further study is needed to obtain stable P/E cycles. Long read pulse endurance of >106 cycles is shown in Figure 6b. In this case, stress pulse width was 500 μs and read pulse width was 10 μs. Stable LRS

is obtained at a V read of 0.1 V. Due to the strong conducting filament formation, stable LRS is observed under random read pulse. For LRS only, it took a long measurement time of approximately 3 days. On the other hand, the data retention is quite good after programming the device. The HRS was read out at two different V read’s of Idasanutlin in vivo +0.1 and +0.05 V. Stable HRS is observed up to 400,000 cycles, and the HRS is decreased with pulse numbers. This may be due to defects creation during continuous AZD2014 mouse stress on the TaO x switching layer or the migration of oxygen ions

due to heating effects. Further study is needed to improve P/E endurance and instability of read pulse endurance of HRS after long cycles. However, a check details resistance ratio of >10 is obtained after 106 cycles. Our memory device also performs good data retention of >104 s as shown in Figure 7. The read voltage for both HRS and LRS was −0.2 V. An acceptable resistance ratio of >10 is observed after a retention time of CYTH4 104 s. This RRAM device is very useful for nanoscale non-volatile memory application. Figure 6 Endurance characteristics. (a) P/E

endurance of >103 cycles and (b) long read pulse endurance of >106 cycles of our novel W/TaO x /TiN memory device. The device size is 4 × 4 μm2. Figure 7 Data retention characteristics. Good data retention of >104 s of our W/TaO x /TiN memory device. An acceptable resistance ratio of >10 is obtained after 104 s. Conclusions One hundred consecutive switching cycles in the W/TaO x /TiN structures under self-compliance (<200 μA) and low-voltage operation of ±2.5 V are obtained. The thicknesses of TaO x and TiO x N y layers are 7 and 3 nm, respectively, which are observed by HRTEM. The RRAM device sizes are also confirmed by TEM. Our memory device shows good switching characteristics at low self-current compliance with tight distribution of HRS/LRS, excellent device-to-device uniformity, and program/erase endurance of >1,000 cycles. The smaller size devices show better switching characteristics and uniformity as compared to the larger size devices, owing to the thinner W electrode as well as higher series resistance. Interfacial oxygen-rich TaO x layer acts as a series resistance to control the resistive switching characteristics which may also cause the self-compliance resistive switching behavior and non-linear I-V curve at LRS. Switching mechanism is based on the formation and rupture of oxygen vacancy conducting path in the TaO x switching material.

For strain 3841, mutation of flaE and flaH resulted in a reduction in swimming motility,

suggesting that these subunits probably contribute to the flagellar filament. However, FlaE and FlaH peptides were not detected in the wildtype flagellar preparations, indicating learn more that these peptides may not be stable under the conditions used. SAHA HDAC Glycosylation of flagellin subunits We observed that for strain 3841, both the upper and the lower bands on the protein gel contained the same set of flagellin subunits (FlaA, FlaB, and FlaC) (Table 3). The molecular masses (around 35kDa; Additional file 3) of the bands observed on the gel also appeared to be higher than the predicted molecular masses (31kDa) for FlaA and FlaB. This suggests that at least FlaA and FlaB may have undergone post-translational modification, resulting in a higher molecular weight and subsequently slower migration in the protein gel. Analysis

of the flagellin amino acid sequences of R. leguminosarum (Fig. 1 &2) revealed the presence of two to four putative glycosylation signals (N-X-S/T, where X is any amino acid except proline) [55]. The MS/MS spectral data for the identified peptides containing the glyosylation signal were also analyzed for the presence of glycosylation, based on the presence of peaks (m/z) corresponding to selleck screening library different types of glycosylation (Additional file 4 shows a sample of a MS/MS spectrum). However, we have not identified any potential glycosylation for these peptides which may be attributed to the lability of this modification

[56, 57]. Also, sequence coverage only ranged from 18% to 46% (Fig. 1 and 2) and peptides at the C-termini of the flagellin subunits were not detected. The C-terminus contains a common glycosylation Buspirone HCl site for the R. leguminosarum flagellin subunits but these glycosylations were not detected in the MS/MS analysis, which could be due to the above reason. Thus, we performed glycoprotein staining to determine if the flagellins are post-translationally modified by glycosylation. We observed positive staining for the flagellins of both VF39SM and 3841 suggesting that these flagellins are glycosylated (Fig. 6). We were unable to determine which flagellins are glycosylated because the seven flagellins were not separated on the protein gel. Glycosylation of flagellins has been reported in a number of animal and plant pathogens including Campylobacter jejuni [56, 57], Helicobacter pylori [57, 58], Pseudomonas aeruginosa [59, 60], Pseudomonas syringae [61, 62], Listeria monocytogenes [63, 64], A. tumefaciens [6], Acidovorax avenae [65], as well as in the nitrogen-fixing bacterium Azosprillum brasilense [66]. It has been suggested that glycosylation may play a role in flagellar filament assembly and in pathogenesis [67, 68].

33, 3.16, 2.90, 2.65, and 2.5, and of 3.32, 3.15, 2.91, 2.65, 2.49 eV, respectively (see Figure 3b,c). These results show that an increase in anodizing voltage from 100 to 115 V leads a rather equal amount of redshift in the position

of all the PL emissions, see for instance peaks 1 and 2 in Figure 3a,b. Figure 3 Fitted PL emission spectra of the aluminum oxide membranes of Figure 2 . The membranes are anodized at (a) 100, (b) 115, and (c) 130 V. In Figure 3a, the 415-nm peak reveals the maximum emission intensity. This emission wavelength is close to the beginning of the blue region. However, the maximum emission locates about 427 nm in Figure 3b,c, which is close to the middle of the blue region. This wavelength shift can slightly improve the PL activity of the membranes in the visible range. In Figure 3c, peak positions show negligible shift compared with Figure 3b. A tolerance error should be considered for Selleckchem INCB024360 both PL measurement and graph fitting procedures because the fluorescence spectrophotometer precision lies at approximately 0.1 nm, and there exists a possibility of error in the fitting process. Consequently, it could be deduced that an increase in the anodizing voltage beyond 115 V has insignificant shifting

effect on the emission spectrum IWR-1 solubility dmso (see Figure 3b,c). These findings indicate that an increase in the anodizing voltage beyond 115 V cannot enhance the PL activity of the membranes

in the visible range. Most of the previous reports have related the PL properties of PAAO layers to the optical transitions within individual oxygen vacancies. However, there is a clear-cut distinction between their interpretations on the type of the oxygen vacancies. Some researches claim in their articles that the PL spectra are concerned to the singly ionized oxygen vacancies [12, 13, 15]. But others relate the spectra to both singly ionized and neural oxygen vacancies [11, 14]. Singly ionized oxygen vacancies are generally called F+ centers. These point defects form when an electron is trapped in a double ionized oxygen vacancy. Neutral oxygen vacancies are often called F centers. They can be formed if SPTLC1 two Sepantronium in vivo electrons are trapped in a double ionized oxygen vacancy. Our results could not confirm the interpretations of the first group; otherwise, our results would not agree with the results on crystalline Al2O3. According to Lee and Crawford studies on sapphire [19] and Evans and coworkers on crystalline α-Al2O3[20], if crystalline Al2O3 is excited under a 4.8 eV (260 nm) wavelength, it would emit UV PL radiation due to the F+ color centers at approximately 3.8 eV (326 nm). Only one PL emission about 3.8 eV is fitted out among our results (see the 323-nm peak in Figure 4c). But several visible emissions far greater than 323 nm are identified (Figure 3a).

[http://​www.​jacmp.​org/​index.​php/​jacmp] J Appl Clin Med Phys 2008, 9: 2792–2799.PubMed 16. Mackie RT, Liu HH, McCullough EC: Treatment Planning Algorithms: Model-based Photon Dose Calculations. In Treatment Planning in Radiation Oncology. 2nd GW4869 cell line edition. Edited by: Khan FM. USA: Lippincott Williams and Wilkins Press; 2007:63–77. 17. Oelfke U, Scholz C: Dose Calculation Algorithms. In New Technologies in Radiation Oncology. 1st edition. Edited by: Schlegel W, Bortfeld T, Grosu A-L. Berlin, Germany: Springer-Verlag Press; 2006:187–196. 18. Fippel M: Monte Carlo Dose Calculation for Treatment Planning. In New Technologies

in Radiation Oncology. 1st edition. Edited by: Schlegel W, Bortfeld T, Grosu AL. Berlin, Germany: Springer-Verlag Press; AMN-107 research buy 2006:197–206.CrossRef 19. Chung H, Jin H, Dempsey JF, Liu C, Palta J, Suh TS, Kim S: Evaluation of surface and build-up region dose for intensity-modulated radiation therapy in head and neck cancer. Med Phys 2005, 32: 2682–2689.CrossRefPubMed 20. Ramsey CR, Seibert RM, Robison B, Mitchell M: Helical tomotherapy superficial dose measurements. Med Phys 2007, 34: 3286–3293.CrossRefPubMed 21. Cheek D, Gibbons JP, Rosen II, Hogstrom KR: Accuracy of TomoTherapy treatments for superficial

buy Gemcitabine target volumes. Med Phys 2008, 35: 3565–73.CrossRefPubMed 22. Roland TF, Stathakis S, Ramer R, Papanikolaou N: Measurement and comparison of skin dose for prostate and head-and-neck patients treated on various IMRT delivery systems. Appl Radiat Isot 2008, 66: 1844–1849.CrossRefPubMed 23. BCKDHB Mutic S, Low

DA: Superficial doses from serial tomotherapy delivery. Med Phys 2000, 27: 163–165.CrossRefPubMed 24. ICRP 2007: The 2007 Recommendations of the International Commission on Radiological Protection: adopted by the Commission in March 2007. Essen, Germany: Elsevier Press; 2007. 25. ICRU 39: Determination of dose equivalents resulting from external radiation sources. Bethesda, MD: International Commission on Radiation Units and Measurements Press; 1985. 26. Landau D, Adams EJ, Webb S, Ross G: Cardiac avoidance in breast radiotherapy: a comparison of simple shielding techniques with intensity-modulated radiotherapy. Radiother Oncol 2001, 60: 247–255.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions FA conceived of the study, coordinated the study, edited and verified the external surface of the patient and lung contours, delineated target volumes, helped acquisition of data, performed the statistical analysis and draft the manuscript. YO has performed treatment plans, participated in acquisition of data and helped to draft the manuscript. RD edited and verified the external surface of the patient and lung contours, delineated target volumes, participated in acquisition of data and helped to draft the manuscript.

It is significant to note that the two predominant amino acids produced in electric discharge experiments are glycine and alanine, the Strecker synthesis products of formaldehyde and acetaldehyde, respectively (Miller 1955). As suggested by Van Trump and Miller (1972), acrolein may have also played a key role as

a GSK2118436 purchase precursor in the formation of glutamic acid, homocysteine, homoserine and α,γ-diaminobutyric acid. Fig. 3 Prebiotic synthesis of methionine, methionine sulfoxide, methionine sulfone, ethionine, and homocysteic acid in the presence of acrolein, which is based in part on the scheme proposed by Van Trump Bucladesine molecular weight and Miller (1972). Asterisks denote species that were detected in this study It has been suggested

that the reaction of ammonium thiocyanate, thiourea, and thiacetamide (all of which are produced from electric discharges acting on NH3, CH4, H2O, and H2S gas mixtures (Heyns et al. 1957)) with formaldehyde can lead to the production of glycine, cysteine, and cystine (Herrera 1942; Perezgasga et al. 2003). It has also been shown that H2S, together with pyrite and other metal sulfides, can partake in surface-mediated reactions that provide electrons for the reduction of organic compounds under simulated volcanic conditions (Huber et al. 2010; and references therein). However, organic sulfur-containing amino acids and amines, such as homocysteic acid, cysteamine, taurine (HO3SCH2CH2NH2) (Choughuley and Lemmon 1966), cysteine (Khare and Sagan 1971; Sagan and Khare 1971) and methionine, seem to be produced more readily

from model H2S-containing primitive atmospheres than from pyrite/metal selleck chemicals llc sulfide reactions (Huber et al. 2010). Two alternative pathways can be suggested for the production of cysteine from glycine under possible prebiotic conditions (Fig. 4). As suggested by Weber and Miller (1981), S-methylcysteine could have formed under primitive conditions by the Michael addition of CH3SH to dehydroalanine (Fig. 4). We could not confirm the formation of dehydroalanine because it is very reactive and thus if present its levels could be below our detection limits, which are in the low femtomole range. The notion that methionine is a product of the addition of CH3SH to acrolein DNA Damage inhibitor (Van Trump and Miller 1972) is supported by the tentative detection of ethionine (Fig. 3), which could have been formed in part by the addition of ethane thiol (CH3CH2SH) to acrolein. Cysteamine has also been produced in a model reducing atmosphere with electron beams, albeit in low yields (Choughuley and Lemmon 1966). Several of the compounds we have detected are known decomposition products of cysteine and methionine. Cysteamine, the simplest aminothiol, is produced by the decarboxylation of cysteine (Fig. 4), and methionine sulfone and methionine sulfoxide are produced by the oxidation of methionine (Lieberman et al. 1965).

65 hours. The mean Vss was 20.1 L, and the CL was 598.3 mL/min. The active metabolite M3 showed a biphasic decline in concentration after reaching Cmax values (mean t½ 1.69 hours), whereas the decline of M4 STAT inhibitor appeared monophasic (mean t½ 0.52 hours). The concentrations of these metabolites were substantially lower than those of bendamustine. The concentrations of the dihydrolysis product HP2 were initially also much lower than the concentrations of bendamustine but, unlike the other analytes, small but measurable

levels of HP2 were still present at 24 hours after the start of the infusion, with a mean concentration at 24 hours check details of 3.75 ng/mL. The TRA concentrations were characterized by a very slow decrease after reaching Cmax values. After 168 hours, the mean

TRA concentration was still 2.29 μg Eq/mL, and the mean t½ of the apparent terminal phase was estimated at 197 hours (Table 2). Bendamustine, M3, M4, and HP2 composed the bulk of the TRA early in the profile (almost 80%); however, their contribution to the TRA quickly declined to approximately 1% at 4 hours after the start of the infusion. PF-02341066 cost The mean concentration ratio of TRA in plasma and in whole blood (Fig. 3) was ~1.4

immediately after the end of the infusion and approximately 1 at later time points. Fig. 3 Mean (±standard deviation) [n = 4–6] plasma to whole-blood concentration ratio of total radioactivity immediately after the end of a 60-minute (120 mg/m2, 80–95 μCi) 14C-bendamustine hydrochloride infusion and at Amisulpride weekly time points thereafter. TRA total radioactivity 3.3 Excretion Balance For all six patients, urine and fecal samples were collected as planned during the first 168 hours after administration of 14C-bendamustine. Thereafter, urine and feces continued to be collected for longer periods in five and three patients, respectively, for up to 3 weeks. Figure 4 shows the mean cumulative urinary, fecal, and total recovery of TRA during 168 hours after 14C-bendamustine administration. At this point, approximately half (45.5%) of the administered radioactivity was recovered in urine and a quarter (25.2%) in feces, resulting in total recovery of 70.6% after 168 hours. After the extended collection period, the total recovery was increased to 76.0%. Individual excretion values are tabulated in Table 3. Fig.

Biomaterials 2012, 33:8848–8857.CrossRef 13. Yang C, Jiang L, Bu S, Zhang L, Xie X, Zeng Q, Zhu D, Zheng Y: Intravitreal administration of dexamethasone-loaded PLGA-TPGS nanoparticles for the treatment of posterior segment diseases. J Biomed Nanotechnol 2013,9(9):1617–1623.CrossRef 14. Fox ME, Szoka FC, Frechet AMJ: Soluble selleck kinase inhibitor polymer carriers for the treatment of cancer: the importance of molecular architecture. Acc Chem Res 2009, 42:1141–1151.CrossRef 15. Cuon NV, Li YL, Hsieh MF: Targeted delivery of

doxorubicin to human breast cancers by folate-decorated TPCA-1 clinical trial Star-shaped PEG–PCL micelle. J Mater Chem 2012, 22:1006–1020.CrossRef 16. Zhang ZP, Tan SW, Feng SS: Vitamin E TPGS as a molecular biomaterial for drug delivery. Biomaterials 2012, 33:4889–4906.CrossRef 17. Zhang ZP, Mei L, Feng SS: Vitamin E d-a-tocopheryl polyethylene glycol 1000 succinate-based nanomedicine. Nanomedicine 2012,

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polyglycerol core. Macromolecules 2010, 43:6671–6677.CrossRef 22. Maglio G, Nese G, Nuzzo M, Palumbo R: Synthesis and characterization of star-shaped diblock poly(ϵ-caprolactone)/poly(ethylene oxide) copolymers. Macromol Rapid Commun 2004, 25:1139–1144.CrossRef 23. Lapienis G: Functionalized star-shaped polymers having PEO and/or polyglycidyl arms and their properties. Polymer 2009, 50:77–84.CrossRef 24. Nabid MR, Rezaei SJT, Sedghi R, Niknejad H, Entezami AA, Oskooie HA, Heravi MM: Self-assembled micelles of well-defined pentaerythritol-centered amphiphilic A4B8 star-block copolymers based on PCL and PEG for hydrophobic drug delivery. Polymer 2011, 52:2799–2809.CrossRef 25. Koyama Y, Ito T, Kimura T, Murakami A, Yamaoka T: Effect of cholesteryl side chain and complexing with cholic acid on gene transfection by cationic poly(ethylene glycol) derivatives. J Control Release 2001, 77:357–364.CrossRef 26. Mehnert W, Mäder K: Solid lipid nanoparticles, production, characterization and applications. Adv Drug Delivery Rev 2012, 64:83–101.CrossRef 27. Mei L, Zhang Y, Zheng Y, Tian G, Song CX, Yang DY, Chen HL, Sun HF, Tian Y, Liu K, Li Z, Huang L: A novel paclitaxel-loaded poly(ϵ-caprolactone)/pluronic F68 nanoparticle overcoming multidrug resistance for breast cancer treatment. Nanoscale Res Lett 2009, 4:1530–1539.CrossRef 28.

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Cellular proliferation is regulated by protein complexes composed of cyclins and cyclin-dependent kinases (cdks). Five major families of cyclins (termed A, B, C, D, and E) have been isolated and characterized. Cyclin D1 reaches it peak of synthesis and this website activity during the G1 phase, and is believed to regulate the G1-to-S phase transition [8, 9].

Cyclin D1 plays a role in DNA repair. Cyclin D1 could bind directly RAD51, a recombinase that drives the homologous recombination process [10]. Cyclin D1 gene is located in the chromosome 11q13 [11]. The expression of cyclin D1 and other cyclins has been often evaluated in many cancers and its prognostic value is disputable. In esophageal squamous cell carcinoma and hepatocellular carcinoma the expression of CyclinD1 has been reported Selleck Sapanisertib to be associated with poor outcomes [12–14]. The aim

of this study was the evaluation of correlations between clinicopathological findings and cyclin D1 and galectin-3 expression in non-small cell lung cancer. We wanted also to analyze the prognostic value of SNX-5422 datasheet cyclin D1 and galectin-3 expression. Moreover we tried to evaluate the correlations between galectin-3 and cyclin D1 expression in tumor tissue. Materials and methods The 47 patients with non-small cell lung cancer (32 men and 15 women) were evaluated. The mean age of the patients was 59.34 ± 8.90 years. All patients had undergone the surgical treatment (lobectomy, bilobectomy, pneumonectomy or diagnostic thoracotomy). The histopathologic diagnosis was squamous cell carcinoma in 24 patients, adenocarcinoma in 15 patients, large cell carcinoma in 4 patients and non- small cell lung cancer of unspecified type in 4 patients. Based on the TNM staging system: 17 patients were in stage I (including IA-5 persons,

IB-12), C59 datasheet 8 in II (IIA- 1, IIB-7), 16 in III (IIIA-13, IIIB-3) and in 6 IV. Twenty-one patients received chemotherapy-treatment, in this group 12 persons neoadjuwant chemotherapy. In all patients the 24 month survival has been evaluated. Twenty seven (57.45%) patients were alive and 20 (42.55%) died. The average survival time was 18.91 ± 7.14 months. The work has been approved by the appropriate ethical committees related to the institution. Immunohistochemistry Formalin -fixed well preserved tumor tissue blocks from surgically resected lung cancer specimens were used for immunohistochemical study. The 4 μm-sections of formalin -fixed tissues were mounted on silanized slides, deparaffinized in xylene and rehydrated through serial baths of alcohol to water. The hydrated sections were treated in 3% hydrogen peroxide for 10 minutes to eliminate endogenous peroxidase activity and washed in phosphate-buffered saline (PBS).