HPV infections with mucosal types are very common, especially in young women. Most natural HPV infections are cleared through an immune response in which two pathways can be differentiated. Firstly, the humoral response leads to the production

of neutralizing antibodies, which will prevent the virus to enter the epithelial cell. This immune response takes approximately 6 to 18 months to mount and serological levels are low, with approximately 70% of individuals raising detectable levels of antibodies against a type-specific L1 epitope [18]. These antibodies, although useful in the prevention of primary infection of basal keratinocytes, are insufficient to prevent new infections. Secondly, the HPV enters the cell through contact with the basal membrane and through the interaction with alpha-6 Panobinostat ic50 integrin, which is a natural component of the hemidesmosal complex that binds the epithelial cell to the basal membrane [19]. More specifically, the L1 part of the virus binds to laminin-5. Thereafter, the virus is transferred to alpha-6 integrin and

internalized. The internalization process is still not completely understood [20]. After internalization, the epithelial cell sheds the capsid, losing L1 and L2, explaining the difficulty for the Idelalisib nmr type-specific anti-L1 antibodies to react. The cellular clearance of HPV is therefore dependent on cytotoxic T cells that react with infected cells through the recognition of expressed viral proteins (like E6 and E7) [19]. Genital HPV infection is therefore associated with a defective Th1 profile and an increase of the permissive Th2 profile of cytokine production [21]. Indeed, both experimentally as well as clinically, cellular clearance of HPV infection

is linked to a Th1 cytokine response and cytotoxic T lymphocytes, raised against HPV epitopes can eradicate HPV-related tumours. Finally, this mechanism forms the basis of therapeutic vaccines as discussed later in this paper. The commercially available vaccines are constructed using virus-like particles (VLPs) that consist of L1. It is widely accepted, but clinically only proven in animal experiments, that these vaccines protect by invoking an antibody response [18]. This serological Non-specific serine/threonine protein kinase response is much stronger (1–4 logs higher) than the response towards a natural infection, which is likely due to the use of specific adjuvants, the strong immunogenicity of the VLPs themselves, as well as the route of administration. In vaccinated individuals, an adaptive immune response is induced after intramuscular injection. Most research is done looking at IgG antibodies, specifically raised against type-specific L1 proteins. As the capsule of the natural HPV virion also expresses the L2 protein, using L2 VLPs is currently being investigated and promising but technically more challenging (see later). The L1 IgG is expressed in the cervical mucus, suggesting a role for immediate neutralizing of the virus.

8 kg), powdered and exhaustively extracted with ethanol (95%) on a steam bath for 8 h thrice. The extract was concentrated under reduced pressure and left overnight at room temperature when a light brown solid deposited at the bottom of the flask. This ethanolic extract residue (4.5 g) was dried and the mother compound screening assay liquor on concentration in vacuum using rotary flash evaporator afforded a dark brown semi-solid (104.5 g) which was successively re-extracted with pet. ether (60–80%) followed by dichloromethane which on concentration afforded dark brown solids (2.4 g

and 5.3 g respectively). Since the pet. ether and dichloromethane fractions exhibited a similar TLC profile (benzene:ethyl acetate, 1:1), they were mixed together for further studies. The ethanolic extract residue was chromatographed on an open normal silica column (h × Ø = 40 × 2 cm) eluted with pet. ether with increasing PF-06463922 mouse amount of EtOAc affording n-hexacosane (0.198 g), polypodatetraene

(semi-solid), α-amyrin acetate (0.159 g), gluanol acetate (0.356 g), lupeol acetate (0.216 g), β-amyrin acetate (0.198 g) and bergenin (0.251 g). The pet. ether and dichloromethane fractions on column chromatography yielded 24,25-dihydroparkeol acetate (0.224 g), lanost-22-en-3β-acetate (0.175 g), gluanol acetate (0.229 g), lupeol acetate (0.140 g), α-amyrin octacosanoate (0.162 g), β-sitosterol (0.128 g) and β-sitosterol-β-D-glucoside (0.056 g) ( Fig. 1). The DPPH radical scavenging activity was determined by the method of Fogliano et al.9 A solution (2.5 ml) of 2 × 10−3 μg/ml of 2,2-diphenyl-1-picrylhydrazyl (DPPH) in methanol was mixed with equal volume (2.5 ml) of extract/test compound/ascorbic acid (standard) at different concentrations (10, 20, 40, 60, 80 μg/ml) in methanol. The mixture was shaken vigorously, and then kept in dark for 30 min. The absorbance was monitored at 517 nm using UV–Vis spectrophotometer. Blank was also carried out to determine the absorbance of DPPH, before interacting with the sample. The IC50 is the concentration of an antioxidant at which 50% inhibition of free radical activity Bay 11-7085 is observed. The decoloration i.e. DPPH scavenging effect (% inhibition)

was plotted against the sample extract concentration and a logarithmic regression curve was established in order to calculate the IC50. Fe3+ – Fe2+ transformation assay was carried out by Oyaizu’s method.10 To 1 ml of extract/test compound/ascorbic acid (standard) at different concentrations (62.5, 125, 250, 500, 1000 μg/ml) in ethanol was added 1 ml of distilled water, 2.5 ml phosphate buffer (0.2 M, pH 6.6) and 2.5 ml potassium ferricyanide (1%). The mixture was incubated at 50 °C for 20 min. Trichloroacetic acid (2.5 ml, 10%) was added to the mixture, which was then centrifuged for 10 min. The upper layer of solution (2.5 ml) was mixed with distilled water (2.5 ml) and FeCl3 (0.5 ml, 0.1%) and the absorbance was measured at 700 nm using UV–Vis spectrophotometer.

A p value ≤ 0.05 was deemed to be statistically significant. A

paired t-test with Bonferroni correction was used (with p = 0.05/6 = 0.0083) for the pair-wise comparison in muscle activity and marker displacement in the frontal and sagittal planes for the two feedback conditions. Nineteen participants were recruited from the Department of Physical Therapy, Yonsei University, Selleck IBET762 Korea. The characteristics of the participants are presented in Table 1. All participants completed all aspects of the testing procedure according to the random allocation of testing conditions. For the upper trapezius muscle, the main effects were significant for shoulder flexion angle (p < 0.001) and feedback (p = 0.017), as was the interaction effect (p = 0.003). Visual feedback increased activation of the upper trapezius at both 60°

and 90° of shoulder flexion ( Table 2). After Bonferroni correction, however, the effect of visual feedback was significant only at the 60° shoulder flexion angle (p = 0.008). For the lower trapezius muscle, the main effect for shoulder flexion angle was significant (p = 0.001), but neither the main FRAX597 chemical structure effect for the visual-feedback condition (p = 0.152) nor the interaction effect (p = 0.150) was significant. The data are presented in Table 2. For the serratus anterior muscle, the main effects were significant for shoulder flexion angle (p < 0.001) and feedback

(p < 0.001), as was the interaction effect (p = 0.045). Visual feedback significantly increased activation of serratus anterior at both 60° and 90° of shoulder flexion ( Table 2). After Bonferroni correction, the effect of visual feedback remained significant at both 60° and 90° of shoulder flexion (p < 0.001). Measurement of displacement of the acromial marker in the frontal plane showed that the average movement was superior for all combinations of flexion angle and feedback. The main effects were significant for shoulder flexion angle (p < 0.001) and feedback Mephenoxalone (p < 0.001), as was the interaction effect (p = 0.001). Visual feedback significantly increased the superior displacement of the acromion ( Table 3). After Bonferroni correction, the effect of feedback remained significant only at 60° of shoulder flexion (p < 0.001). Measurement of displacement of the acromial marker in the sagittal plane showed that the average movement was anterior with feedback and posterior without feedback. The main effect was significant for the visual feedback (p = 0.000), but neither the main effect for shoulder flexion angle (p = 0.100) nor the interaction (p = 0.268) was significant. After Bonferroni correction, the effect of visual feedback on anterior movement of the acromion during shoulder flexion remained significant at both 60° and 90° of shoulder flexion (p < 0.001).

Briefly, OMVs from serogroup B meningococci were adsorbed to fluorescent polystyrene latex microspheres (Fluoresbrite Plain Microspheres, Polysciences, Warrington, Pennsylvania) of approximately size of meningococci (1 μm of diameter). FITC was incorporated within the polymer, leaving the surface free to adsorb

the protein. The latex beads (500 μl, 4.55 × 1010 beads/ml) AZD8055 were centrifuged at 15,600 × g for 5 min, and the pellet was suspended in a 940 μg/ml solution of OMV in 0.1 M borate buffer (0.1 M boric acid, adjusted to pH 8.5) followed by end-to-end rotation overnight (20 h) at 20 °C. After additional blocking of unreacted sites on the OMV beads with 2% bovine serum albumin (BSA) in 0.1 M borate buffer, the OMV-bead pellet was suspended in storage buffer (0.1 M phosphate buffer, containing 5% glycerol, 0.02% merthiolate and 1% BSA, pH 7.4), and kept protected from daylight in aliquots

at 4 °C until used. The antigen coated bead suspensions (100 μl, 3.3 × 108 beads/ml) were opsonised for 8 min with 25 μl of diluted test serum (1:20) previously heat inactivated at 56 °C for 30 min, with a total sample volume of 400 μl obtained by addition of PBS–BSA, supplemented with CaCl2 (0.98 mM) and MgCl2 (1 mM). 25 μl of human serum that lacked detectable intrinsic opsonisation activity diluted at 1% was added to the reaction and were incubated with end-to-end rotation for 8 min at 37 °C. Donor leukocytes (100 μl, 1.25 × 107/ml) were added and the suspensions over were incubated for 8 min. Phagocytosis was terminated by adding 1.5 ml of ice-cold PBS supplemented with 0.02% EDTA. The suspensions were kept on ice until analyzed GDC-0199 price by a FACScalibur flow cytometer [16]. The levels of significance of the differences between groups were examined by Paired or Unpaired t test (parametric tests) For nonparametric data we used Mann–Whitney test (unpaired samples) or Wilcoxon matched pair test (paired samples). These analyses were performed with a GraphPad-Prism software, version 4.02. P < 0.05 was taken as significant. Fig. 1A shows the percent of specific

memory B-cells detected as specific ASC after in vitro stimulation of peripheral blood memory B-cells for 6 days. Memory B-cells were detected only in one individual 7 days after the first dose (0.5%) and in 2 individuals at 14 days (mean of 0.16%). A significant memory B-cell response was seen 7 days (mean of 0.27%) and 14 days (mean of 0.46%) after the third vaccination. At this time, memory B-cells were detected in all individuals, with frequencies varying from 0.14 to 0.95%. A significant decrease of memory B-cells was recorded 6 months (mean of 0.03%) later (pre-booster). Surprisingly, 14 days after the booster dose, only 2 of 5 individuals responded with an increase in memory B-cell frequencies with values of 0.15% and 0.34% (mean of 0.1% for all individuals). As can be seen in Fig. 1B, we observed a continuous and gradual decrease (P > 0.

The specimens and questionnaires were anonymous, and feedback was given to all participants of the study, including their results. All unprotected participants were advised to be vaccinated against hepatitis A. Data are presented as medians and frequencies. The performance of the laboratory tests with the collected oral fluid samples was determined by comparing the sensitivity, specificity, and positive and negative predictive values and their respective 95% confidence intervals RAD001 clinical trial (95% CI) with the serum results, which

were used as a gold standard control. The linear and weighted kappa (k) statistic was used to evaluate the rate of agreement between the oral fluid and serum anti-HAV antibody status for each device used. According to the strength of the agreement, the k value was interpreted as follows [16]: <20%: poor; 21–40%: fair; 41–60%: moderate; 61–80%: good; and 81–100%: very good. To compare proportions, the Chi-square (χ2) test for independence with selleck screening library Yate’s continuity correction, χ2 for trend, and Fisher’s exact test

(when appropriate) were used. The Spearman’s coefficient of rank correlation (rs) was used to evaluate the degree of the relationship between the values of color intensity on the colorimetric scale obtained after using the oral fluid collection devices. A two-tailed p < 0.05 was considered statistically significant. All analyses were performed with MedCalc for Windows, version

8.1.0.0 (MedCalc Software, Mariakerke, Belgium), and GraphPad InStat version 3.05 (GraphPad Software, CA, USA) software. The optimal oral fluid dilution for detecting anti-HAV antibodies in the ImmunoComb® II HAVAb was determined using matched samples from the optimization panel. Among the 30 individuals with natural immunity to HAV, oral fluid samples collected by OraSure® and Salivette® devices presented concordant results with those from serum samples until a 1:25 dilution. However, false-negative results were observed after TCL the 1:5 dilution when the ChemBio® device was used. For the 25 HAV-vaccinated individuals, all of the diluted samples presented false-negative results, irrespective of the oral fluid collection device used. False-positive results were not observed in the group of 35 individuals who were non-reactive for anti-HAV antibodies. Based on these findings, the detection of anti-HAV antibodies by all of the devices was optimal when undiluted oral fluids were used; the evaluation of other parameters (temperature, incubation time, etc.) was not required to optimize these samples. The rate of agreement between the oral fluid and serum anti-HAV antibody status for each device was evaluated for each group of individuals.

Delegates from the countries subsequently presented these data at the international workshop. This document provides a summary of the workshop and outlines the presented results and the recommendations from the meeting. Surgeons from 13 hospitals representing 10 African

countries attended the meeting. Countries represented at the meeting included: Botswana, Cote D’Ivoire, Ghana, Kenya, Malawi, Nigeria, South Africa, Tanzania, Zambia and Zimbabwe. In all countries except South Africa and Botswana, the data were collected from hospital records at the largest paediatric hospital in the capital city of each country. In South Africa, Bcl-2 inhibitor we collected data from three large academic hospitals in three cities. In Botswana, a review of hospital data was performed by a single surgeon from two government hospitals. From 1993 to 2003,

a total of 1069 case-patients with intussusception were treated at the 13 hospitals represented at the meeting. Age data were available on 729 infants with intussusception (Fig. 1). The age distribution of intussusception in the 10 African countries was similar to that in the published literature from other regions of the world, with 13% of the burden among infants <3 months of age, 56% among infants 4–6 months, 23% among infants 7–9 months, and 8% among infants 10–12 months of age. Intussusception events occurred during most months of the year, without any evident seasonal click here Oxymatrine peaks (Fig. 2). The diagnosis of intussusception, clinical management, and outcome was presented from 10 sites. At these sites, the vast majority of intussusception case-patients were diagnosed surgically (69%) some at autopsy. Contrast enema and ultrasonography were used to diagnose intussusception only in 10% and 11% of the case-patients,

respectively. Surgical treatment (reduction or resection) was employed in 90% of the case-patients. In six countries that specified the proportion that required resection, this varied from 27% in Kenya to 62% in Nigeria. In one analysis in South Africa, resection was performed in 46% of cases at Ga-Rankuwa Hospital over a 20 year period between 1983 and 2003 (L. Marcisz, unpublished data). At the 9 sites with available data on outcome, 108 of 863 (13%) intussusception case-patients died after presentation to the hospital. The past history of rotavirus vaccines has necessitated the consideration of intussusception with all new rotavirus vaccines and WHO has recommended that post-marketing surveillance is implemented in countries that introduce rotavirus vaccines [2] and [8]. Thus, monitoring of intussusception is an important activity after the routine introduction of rotavirus vaccines in national immunization programmes [3] and [14].

In the past, the disease has also spread to Europe, specifically to Spain in 1969 and Spain and Portugal in 1987 [1] and [2]. The latest outbreak in Western Mediterranean countries lasted 5 years [3] and [4]. To date no effective treatment exists for AHS and consequently control of the disease relies on preventive vaccination. AHS vaccines, based on attenuated AHS viruses, have been in use in South Africa for almost 100 years and permitted

the subsistence of horses in that part of the world. There are nine different serotypes of AHS virus (AHSV) and protective immunity is long-lived against homologous serotypes. Thus, vaccination in endemic countries is normally PLX3397 performed by administration of combinations of representative attenuated strains of each of the virus serotypes. Serotypes 5 and 9 are normally excluded from vaccine formulations. Serotype 5 is difficult to attenuate and partially cross-reacts with serotype 8; and serotype 9 does not normally occur in South Africa (the main AHSV vaccine manufacturing country) and partially cross-reacts with serotype 6 [3], [5] and [6]. Despite their apparent efficacy, live AHSV vaccines have a number of disadvantages [4]. These include: (a) the risk of reversion

to virulence; (b) the risk of gene segment re-assortment between field and vaccine strains; (c) the risk of introducing foreign topotypes into a new geographical region, since vaccines are based on South African strains; (d) the absence of DIVA (Differentiating Infected from Vaccinated Animals) capacity, that is the Selleck Ibrutinib inability to serologically differentiate vaccine-induced immunity from that induced by natural infection; and (e) the contra-indications for use in pregnant mares because of their teratogenicity. In addition to these science-based shortcomings of the live vaccines it is also important to consider the potential logistical delays between the first detection of an outbreak and the deployment of sufficient vaccine doses to where they would be needed. The recognised shortcomings of

Phosphoprotein phosphatase existing live AHSV vaccines has meant that alternative vaccination strategies have been pursued over the years. These have included the use of killed vaccines [7], [8] and [9], vaccines based on baculovirus-expressed AHSV capsid proteins [10], DNA vaccines [11] and those based on the use of poxvirus expression vectors [12], [13] and [14]. The latter appear to be a particularly promising strategy, which has started to produce encouraging results. We have demonstrated recently that recombinant MVA viruses expressing VP2 from AHSV serotype 4 (MVA-VP2), the major capsid protein of AHSV and main target of virus neutralising antibodies (VNAb), induced VNAb in horses and complete protection against virulent challenge in a mouse model [12] and [13].

Additional versions: Nil. Expert working group: 16 individuals representing health care professional groups

(medical specialties, nursing, pharmacy), consumers, and guideline developers. Funded by: National Health and Medical Research Council of Australia. The guidelines were developed by the National Institute of Clinical Studies (NICS). Consultation with: External input was indicated in the guideline development process, but Selleckchem Y27632 details were not provided. Approved by: National Health and Medical Research Council of Australia. Location: http://www.nhmrc.gov.au/_files_nhmrc/file/nics/programs/vtp/guideline_prevention_venous_thromboembolism.pdf Description: This is a 157 page document that presents evidence-based recommendations related to the prevention of venous thromboembolis in patients admitted to Australian hospitals. The primary options for thrombophylaxis considered in this guideline were pharmacological and mechanical, which included knee or thigh

length graduated compression stockings, knee or thigh length intermittent pneumatic compression, or venous foot pumps. A 7-page summary of recommendations is provided from page 4. These recommendations are presented by clinical procedure (e.g. total hip replacement), or medical condition (e.g. stroke). Specific recommendations are provided for cancer patients (surgical and non-surgical) and pregnancy and childbirth. There is also a clear 1-page summary of the evidence Selleck R428 for the use of thromboprophylactic agents by clinical category (e.g. abdominal surgery) on page 25. The body of the guideline provides the detailed evidence that underpins the

recommendations, including the level and grade of evidence and the related references. A list of the 392 references included in the document is provided. “
“Latest update: August 2010. Next update: Within 3–5 years. Patient nearly group: Patients aged over 18 years presenting with a stroke or TIA. Intended audience: Health professionals, administrators, funders and policy makers who plan, organise and deliver health care for people with stroke in all phases of recovery. Additional versions: This document updates and amalgamates two previous Australian guidelines: Clinical Guidelines for Acute Stroke Management (2007) and Clinical Guidelines for Stroke Rehabilitation and Recovery (2005). Expert working group: 35 individuals representing 17 health care professional groups including medical specialties, nursing, physiotherapy, occupational therapy, speech pathology, and other professions. Funded by: National Stroke Foundation of Australia, Department of Health & Ageing. Consultation with: Public consultation about the draft document was undertaken over one month, with numerous stakeholder groups specifically targeted for feedback. Approved by: National Health and Medical Research Council of Australia, National Stroke Foundation. Location: http://www.strokefoundation.com.

We also determined the antibacterial activity of the extract against Gram-positive and Gram-negative bacteria. All the solvents and chemicals used in this study were of analytical grade and obtained from HiMedia, Mumbai, India. 2,2-dipicryl-1-picrylhydrazyl (DPPH) was obtained from Sigma Chemical Co., St. Louis, MO, USA. The seeds of C. carvi were obtained from the supermarket located in Ontikoppal, Mysore, Karnataka, India. The C. carvi seeds were

cleaned, powdered and defatted using hexane in a Soxhlet apparatus for 6 h at 47 °C. The defatted C. carvi powder (10 g) was successively extracted with 100 ml water, 100 ml Capmatinib cell line 50% ethanol and 100 ml of equal mixture of 70% aqueous methanol and 70% aqueous acetone by stirring for 2 h at room temperature and the procedure was repeated SCH772984 mouse thrice. All the respective extracts were combined and concentrated under vacuum in a rotary evaporator and subjected to hydrolysis with 2 N HCl to facilitate the breakage of glycosides. Further, the extract was phase separated with hexane

to remove any traces of fatty acids and subsequently with ethyl acetate (1:1) to extract polyphenolic compounds. The ethyl acetate phase was concentrated under vacuum and was kept at 4 °C until use. The total phenolic content of the extracts from three different solvent systems was estimated by Folin–Ciocalteau method.20 The phenolic content was expressed as gallic acid equivalents (GAE) of extract. The radical scavenging

activity of C. carvi phenolic extract was evaluated using DPPH as described earlier. 21 The changes in the absorbance of the samples were measured at 517 nm and the radical scavenging activity was expressed as the inhibition percentage using the following equation, %inhibition=[(O.D.ofblank−O.D.ofsample)/O.D.ofblank]×100 The samples were analyzed in triplicates and the IC50 value was calculated. The superoxide anion radicals were generated in a PMS-NADH system by the oxidation of NADH and assayed Phosphoprotein phosphatase by the reduction of NBT.22 The scavenging activity was calculated using the equation %inhibition=[(O.D.ofblank−O.D.ofsample)/O.D.ofblank]×100 The samples were analyzed in triplicates and the IC50 value was calculated. The reducing power of C. carvi extract was determined according to the method of Oyaizu. 23 The average values of at least three measurements were plotted and compared with standards, BHA and BHT. The protective property of the C. carvi phenolic extract against oxidatively damaged DNA was determined using calf thymus DNA and analyzed by gel electrophoresis using 1% agarose/TAE buffer, at 60 V for 3 h. The DNA was visualized and photographed using a digital imaging system. The antibacterial activity of C. carvi phenolic extract was tested against food borne pathogens and food spoilage bacteria viz., Bacillus cereus, Escherichia coli, Staphylococcus aureus and Salmonella typhimurium by agar diffusion method with slight modifications.

First, a visual assessment of the emulsion was performed at regular intervals when the formulated vaccines were stored at INCB024360 in vivo 4 °C for 12 months. At the initial time point, the finished emulsions appeared white or as an off-white, opaque liquid. After storage at 4 °C for 1 week, a transparent oil-like layer at the top of the emulsion with a white opaque layer

at the bottom was observed. Following gentle shaking, the two phases were easily combined and again appeared as a white opaque liquid whose drop and conductivity tests were indistinguishable from fresh sample (data not shown). To investigate the integrity of the antigen in the emulsion following storage after 1 year, the protein was extracted and analyzed by SDS-PAGE and Western blot analysis. As shown in Fig. 1, no degradation bands from the emulsion-extracted protein were observed on the SDS-PAGE gels visualized with Coomassie when emulsions were stored at 4 °C for 1 year. Silver staining with extracted protein stored for more than 2 years also showed no degradation (Fig. 2). Finally, the anti-MSP1-19 monoclonal antibody mAb5.2 bound to the entire protein and not to degradation products (Fig. 3). To test the integrity of PfCP-2.9 in emulsions stored at different temperatures,

the vaccine emulsions were stored at 25 and 37 °C for various periods. As shown in Fig 4, the protein extracted from the emulsion was stable for up to

3 months when it was second stored at 25 °C and some degradation was observed DAPT in vivo by SDS-PAGE gel after 1 month storage at 37 °C and degradation increased dramatically after 3 months at this temperature. Some protein aggregation was observed following extraction from emulsion as noted by SDS-PAGE and Western blot analyses. Protein multimers increased over time and as the storage temperature increased (Fig. 2 and Fig. 4). It is likely that protein aggregation was not disulfide band dependent since it was not susceptible to reducing conditions (Fig. 1D, lane R). However, aggregated protein was recognized by mAb5.2 as shown in Fig. 3, indicating that the multimers retained their critical conformational epitope intact. To quantitatively analyze the aggregated protein, we used the gel-HPLC method which allowed for the separation of materials such as proteins or chemical reagents based on their molecular weights. As shown in Fig. 5, the peak pattern in Fig. 5A was for that of the extract from the blank emulsion that lacked the PfCPP-2.9 protein whereas that of the extract from vaccine emulsion containing the protein in Fig. 5B showed two additional peaks (the two additional peaks corresponded to PfCPP-2.9 and PfCPP-2.9 dimers). Analysis of the area under the respective peaks demonstrated 7.6% dimmers and 92.4% monomers.