Electrochemical detection of DNA hybridization usually involves c

Electrochemical detection of DNA hybridization usually involves changes in electrochemical parameters such as; capacitance [15], impedance [16] and electrochemical quartz crystal microbalance measurements [17] at fixed potential or detecting complementary target, using both direct electrochemical oxidation of guanine and redox of the electroactive indicator methylene blue [17], [18] and [19]. The above listed electrochemical DNA-sensors that use label-free probes are cost effective alternatives adopted for real-time monitoring, however

with serious drawbacks; low selectivity and low sensitivity [15] and [17]. This paper describes the use of a capacitive DNA-sensor application, where a surface-bound label-free oligonucleotide probes captures a target complementary DNA-sequence and real time measurement is performed. Nevertheless, the application of elevated temperature to reduce non-specific hybridization (interaction

Selleck ICG-001 of non-complementary oligos) in order to increase the selectivity, the influence of oligo length to the signal strength, and application of sandwich hybridization approach in order to amplify the signal strength of the long DNA molecules are reported. All single stranded oligonucleotides were obtained from Eurofins MWG Operon (Ebersberg, Germany): 25-mer oligonucleotides-C (oligo-C); 15-, 25- and 50-mer oligonucleotides-G (oligo-G); and 25-mer oligonucleotides-T (oligo-T). Absolute ethanol and sodium hydroxide (NaOH) were obtained from VWR International (Leuven, Belgium). Tyramine, N-hydroxysuccinimide (NHS), N-(3-dimethylaminopropyl) N-ethylcarbodiimide Selleck Pifithrin �� hydrochloride (EDC), ethanesulfonic acid (MES), and 1-dodecane thiol were obtained from Sigma–Aldrich (Steinheim, Germany). All other chemicals used were of analytical grade. All buffers and regeneration solutions were prepared with double distilled water from a Milli-Q system (Millipore, Massachusetts, USA). many All solutions were filtered through

a membrane (pore size 0.22 μm) and degassed prior to use. A gold electrode (99.9% purity, custom-made, ϕ = 3 mm) with a surface area of 0.07 cm2 was used as a working electrode. Prior to the modification with oligonucleotides, the gold electrode was polished with alumina slurry with a particle size of 0.1 μm (Struers, Ballerup, Denmark) and cleaned through sonication in distilled water and subsequently in absolute ethanol, for 15 min in each solvent. It was then washed with distilled water and dried with pure nitrogen gas [20], followed by plasma cleaning, PDC-3XG (Harrick, New York, USA) for 20 min, and after that coated by the electropolymerization of tyramine on the electrode surface [21]. The coated electrode was rinsed with distilled water to remove any loosely bound polymer and it was finally carefully dried with pure nitrogen gas prior to immobilizaton.

3–1 m and 1–2 5 m, respectively covering 845, 883 and 476 km2, i

3–1 m and 1–2.5 m, respectively covering 845, 883 and 476 km2, i.e. 2204 km2 in total. About 30 km2 of beaches and dunes are likely to disappear. The greatest impacts of accelerated sea-level rise would occur in the far eastern and western regions of the Polish coast, in the deltas of the Vistula and the Odra, with lesser impacts along the central region.

Threatened areas include the conurbation of Gdańsk, Sopot and Gdynia, the Żuławy (Vistula Delta) polders, and the low-lying areas around the Szczecin Lagoon and the Odra river mouth. These threatened areas are densely populated and of key importance to the Polish economy. The agricultural area of the vulnerable Żuławy polders is about 1800 km2, that is, nearly 0.6% of the total area of Poland. The Hel Peninsula, narrow and low, is already vulnerable in places. This area, of large aesthetic click here and emotional value to the Polish nation, will be increasingly threatened in the decades to come. Flood protection and flood management strategies can modify either flood waters, or susceptibility to flood damage and the impact

of flooding. One can try Staurosporine nmr to ‘keep people away from water’ or ‘keep water away from people’. There are several adaptation strategies for coping with floods (see Kundzewicz & Schnellhuber 2004). They can be labelled as follows: protection (as far as is technically possible and financially feasible, bearing in mind that absolute protection does not exist), accommodation (living with floods, learning from them), or retreat (relocation of people from flood-risky to flood-safe areas). This last option, e.g. if the state/province purchases land and property Thymidine kinase in flood-prone areas, aims to rectify maladaptation and floodplain development. The components of a flood protection and preparedness

system can be divided into five categories, as illustrated in Table 1. These categories are recognised as strategies in the STAR-FLOOD Project (see the footnote on the first page of this paper). One can try to reduce flood risk by structural and technological means (e.g. hard engineering solutions and implementation of improved design standards), or by legislative, regulatory and institutional means (integrated management; revision of guidance notes for planners and design standards). One can avoid or reduce risk by relocation or some other avoidance strategy, by improvements in forecasting systems, and by contingency and disaster plans. One can share loss (insurance-type strategies) but one has to be prepared to take a residual risk. Research (reducing uncertainties) and education on flood risk are essential. Flood defences in Poland are mostly structural and include embankments and storage reservoirs. Those in the Vistula River basin include embankments with a total length of ca 4700 km, protecting an area of ca 5300 km2.

The gi function was obtained by considering these minimum and max

The gi function was obtained by considering these minimum and maximum values. The optimization was performed in order to achieve films with higher resistance to break, moderate elongation, and lower solubility. So the weight of gi functions for elongation was reduced and the weight for TS and S was increased. Thus, the gi functions for TS, E,

and S were assigned weights 3, 1, and 3, respectively (Eqs. (18) and (19)): For glycerol films equation(18) G=[(0.6667−1.118X1+0.45X12+0.48X2−0.10X22−0.35X1X23.9)3×(74.73+26.18X1−11.11X12−10.26X2+2.88X22+8.10X1X298)1×(23+7.42X1−8.46X2+2.05X22+5.10X1X243)3]1/3 For sorbitol films equation(19) G=[(0.998−2.70X1+1.09X12+0.80X2−0.47X1X29.5)3×(54.52+30.86X1−7.33X12−6.11X2+7.39X1X282)1×(29.91−7.57X1−7.93X12−9.52X2−4.46X22+5.41X1X248)3]1/3 Optimization of the desirability function (G) for flour films plasticized Fulvestrant nmr with glycerol and sorbitol shows that films with greater resistant to break, moderate elongation, and lower solubility can be obtained at Cg, Cs, and Tp values of 20.02 g glycerol/100 g flour, 29.6 g sorbitol/100 g flour, and 75 °C, respectively. To validate the optimization

methodology employed in this work, amaranth flour films plasticized with glycerol and sorbitol were prepared using the optimal formulation. TS, E, and S of the flour http://www.selleckchem.com/products/Rapamycin.html films were measured and compared with values predicted by Eqs. (8), (9) and (10) for

the films plasticized with glycerol, and by Eqs. (13), (14) and (17) for the films plasticized with sorbitol. The values of relative deviations revealed good correlation between the predicted and experimental values (Table 3). Films prepared with the optimal formulation were characterized with respect to solubility as well as mechanical, barrier, and thermal properties; water sorption isotherms; and microstructure. Results are summarized in Table 4. Tukey’s test demonstrated that the amaranth flour films plasticized with glycerol and sorbitol differs significantly in terms of moisture content and solubility (P < 0.05). Glycerol films display higher moisture content after conditioning (58% Mannose-binding protein-associated serine protease RH, 48 h), compared to sorbitol films with large sorbitol content. This indicates that glycerol acts as a water-holding agent, while sorbitol acts as a plasticizer with minimum contribution from water molecules. It had been reported that the moisture content of pea starch films also changed little after conditioning when sorbitol was the plasticizer, while addition of glycerol to the latter films promoted a 2–4.5 fold increase in moisture content ( Zhan & Han, 2006). Although glycerol enhances the hydrophilicity of flour films, thus increasing their affinity for water molecules, glycerol films are not readily solubilized in the presence of water, but remain intact even after 24 h.

Eighteen-week-old male Swiss mice were supplied by the Animal Hou

Eighteen-week-old male Swiss mice were supplied by the Animal House of the School of Pharmaceutical Sciences and Chemistry Institute

from University of Sao Paulo. The animals were fed a standard pellet diet and water ad libitum, and before each experimental procedure, the animals were anesthetized with ketamine/xylazine solution (80 mg/kg; 8 mg/kg; i.p.). All procedures were performed according to the Brazilian Society of Science of Laboratory Animals (SBCAL), for proper care and use of experimental animals and approved by the local ethics committee (process GDC-0980 nmr number 196). Five mice were randomly placed in an exposure box and exposed to aerosolized HQ at concentrations of 12.5, 25 or 50 ppm or vehicle (saline solution with 5% ethanol) for 1 h, once a day, for 5 days. An ultrasonic nebulizer (NS®, Sao Paulo, Brazil) was used to nebulize the solutions in the box. According to the manufacture’s information the particle size generated Dasatinib in vitro by the nebulizer is within the range 0.5–10 μm. Two openings at the opposite side of the chamber, relative to the introduction of solutions, allowed the air to seep out. This process was performed in an exhaust hood. It is important to emphasize that concentrations of HQ employed in the current study were lower than those

established for in vivo exposure in the literature ( NIOSH Guideline, 1988 and IPCS-INCHEM, 1994). A dose–response

effect had been previously performed and 5-days exposure was the shortest period to evoke the toxic effect (data not shown). HQ concentrations in the exposure box were determined according to NIOSH, protocol No. 5004. The induction of pulmonary inflammation was performed 1 h after the last vehicle or HQ exposure using a similar exposure box approach. LPS (0.1 mg/ml) was aerosolized for 10 min at a Oxymatrine rate of 1 ml/min. Three hours after LPS inhalation, the animals were anesthetized and arterial blood was collected from the abdominal aorta. The total and differential counts were performed as previously described (Macedo et al., 2006). BALF was collected from vehicle- or HQ-exposed animals to determine the number of migrated leukocytes and concentrations of cytokines as previous described by De Lima et al. (1992). MPO activity was determined in the lung tissue obtained from vehicle- or HQ-exposed animals accordingly to Bradley et al. (1982). Lung of vehicle or HQ exposed mice were surgically removed, frozen in nitrogen–hexane solution, cryosectioned (8 μm thickness) and fixed in cold acetone (10 min). Briefly, sections were incubated overnight with Superblock solution to avoid nonspecific binding.

In GEMINI 2, the maintenance benefit of vedolizumab was consisten

In GEMINI 2, the maintenance benefit of vedolizumab was consistent between patients with previous TNF antagonist failure and in TNF antagonist–naive patients. Observed effects of vedolizumab on disease activity biomarkers were small, but evident, and were consistent with the efficacy data. Effects on CRP concentration in patients with increased CRP levels at baseline were less pronounced than effects seen after TNF antagonist treatment in other studies.28, 29 and 30 The apparently slower CRP reduction kinetics warrant careful consideration. Previously, Sirolimus cell line TNF was reported to exert a direct effect on CRP production by the liver.31 Because vedolizumab, unlike TNF antagonists, does

not antagonize TNF directly and may not affect the mesentery, an important source of CRP in CD,32 it is scientifically plausible to speculate Selleck RG7422 that the reduction in mucosal inflammation resulting from inhibition of leukocyte trafficking causes an indirect (ie, secondary) CRP concentration reduction that occurs gradually, as

seen over the course of 52 weeks in GEMINI 2.24 In contrast, TNF antagonism may result in direct and indirect effects on CRP. Week 6 assessments of fecal calprotectin, a biomarker that has been studied less extensively in CD than in ulcerative colitis (UC), did not show a clinically meaningful difference between treatment groups; however, because these assessments were not conducted at week 10, it is unclear if an effect of vedolizumab would

have become more apparent over time. Future studies are warranted to evaluate the potential healing effects of vedolizumab on the ileocolonic mucosa in patients with CD and to establish an optimal methodology for analysis of drug effects on fecal calprotectin levels in CD. Results of this short-term study support the safety of vedolizumab in patients with CD and are consistent with the Carbohydrate drug’s postulated gut-selective mechanism of action. The safety profile in GEMINI 3 generally is consistent with that in the pivotal trials GEMINI 1 (UC) and 2 (CD), in which no statistically significant differences in treatment-emergent SAE incidences occurred between the vedolizumab and placebo groups.24, 33 and 34 Although upper respiratory tract infection rates were similar between treatment groups in this study, across previous clinical studies, vedolizumab was associated with an increased risk of such infections.24, 33 and 34 This association is potentially consistent with its mechanism of action, namely antagonism of α4β7/MAdCAM-1 interactions in upper respiratory/aerodigestive tract tissues.35 Upper respiratory tract infections with vedolizumab generally have been mild or moderate in severity, requiring no interventions, and an increased risk of lower respiratory tract infections (eg, bronchitis and pneumonia) has not been observed.

The polymerization of the resin subsequently proceeded at 60 °C f

The polymerization of the resin subsequently proceeded at 60 °C for 48 h. The embedded samples were sectioned find protocol in ∼70 nm thick slices using a diamond knife. The sections were transferred to supported gold grids and stained with uranyl acetate and Pb-citrate. The samples were observed under a Carl-Zeiss Model LEO906 transmission electron microscope. The surface-response methodology was used to study the effect of the plasticizer concentration (Cg or Cs) and process temperature (Tp) on dependent variables (mechanical properties and solubility).

The levels of the independent variables were defined according to a 22 full-factorial central composite design (star configuration) (Table 1 and Table 2).

An analysis of variance (ANOVA), a multiple comparison test, and all statistical analyses were performed using the Statistica 6.0 software. The data were fitted to a second order equation (Eq. (2)) as a function of the independent variables. equation(2) Yi=b0+b1X1+b2X2+b12X1X2+b11X11+b22X22where bn are constant regression coefficients, Yi are dependent variables (puncture force (PF), puncture deformation (PD), tensile strength (TS), elongation at break (E), Young’s modulus (YM), and solubility (S)), and X1 and X2 are the coded independent variables (plasticizer concentration and process temperature, respectively). After the surface-response results, were obtained, Ribonuclease T1 optimization

of the process conditions was carried out by multi-response analysis Enzalutamide (Derringer & Suich, 1980). This method involves the transformation of response variables (Yi) to an individual function of dimensionless desirability (gi) (Eq. (4)), ranging from 0 (undesirable response) to 1 (desired response). From the geometric means of individual desires, the overall desirability function (G) (Eq. (3)) is obtained. G was later maximized using the software Mathematic 5.0. equation(3) G=(g1n1,g2n2,……,gknk)1/kwhere: equation(4) gi=Yi−YminYmax−Yminwhere Ymin is the response minimum value and Ymax is the response maximum value, k is the number of considered responses, and ni is the weight of each response. In the case of solubility, Eq. (4) had to be redesigned, so that the minimum values for these responses could be obtained (Eq. (5)). equation(5) gi=Ymax−YiYmax−Ymin Finally, the Tukey’s test was applied at a 5% significance level to compare means for mechanical, solubility, moisture content, barrier properties, and GAB parameters of glycerol and sorbitol films prepared using the optimal formulation. The amaranth flour contains 9.0 ± 0.4 g/100 g moisture, 2.1 ± 0.0 g/100 g ash, 7.9 ± 0.2 g/100 g lipids, 14.1 ± 0.3 g/100 g protein, and 75.8 ± 0.2 g/100 g starch (among which 11.9 ± 0.3 g/100 g was amylose) (dry basis).

, 2006), and data are fit to equations representing a theoretical

, 2006), and data are fit to equations representing a theoretical model associated with selleck chemicals the function under study (e.g., the Michaelis–Menten equation for concentration dependence or Arrhenius equation for temperature dependence). Before computers were readily available, it had been common to first linearize the equation in question, and then conduct a linear root mean square regression (Calcutt and Boddy, 1983 and Skoog et al., 1998) to find the parameters of the model (Segal, 1975). As discussed below (Figure 1) this can lead to erroneous

error propagation, and now that computers and programs that conduct non-linear regressions are readily available, it is always important to conduct non-linear regression to the model under study. Errors that are introduced during the experimental measurement must be propagated throughout the data analysis in order for valid conclusions to be drawn

from the study. Fitting the data to the Michaelis–Menten equation, for example, will have errors associated with kcat, Km and kcat/Km. In a non-competitive assay this will result in individual errors for both the light and heavy isotope that must be propagated when calculating the KIEs using the equations in Table 1. Since multiple measurements have to be made, the final error must be propagated when reporting the KIEs on the different parameters. When measuring KIEs as a function of pH, temperature, pressure, fraction conversion, etc., the errors associated with the individual experiments must be carried over to the fits of the

GSK2118436 order data to the relevant equations. The errors from these fits must be reported when presenting the final fits of the data to obtain the isotope effects reported in the study. The procedures for propagating and reporting errors for KIE data are illustrated Decitabine clinical trial in the examples presented below. Before the widespread availability of software packages that conduct non-linear regression, the kinetic parameters of an enzyme were commonly determined through a linear root mean square regression. Common examples for these procedures included plotting 1/[vo] versus 1/[S] (i.e. Lineweaver–Burk plots), constructing Eisenthal, Cornish-Bowden plots where [S] is plotted on the negative abscissa and vo is plotted on the ordinate, or Hanes–Woolf plots in which the [S]/vo is plotted against [S], where vo is the initial velocity and [S] is the substrate concentration, respectively ( Cook and Cleland, 2007, Cornish-Bowden, 2012 and Segal, 1975). While each method has its advantages and disadvantages, linear regressions of kinetic data result in an erroneous weighing of errors and as a consequence the value and uncertainty of the determined KIE as illustrated in Figure 1 for a hypothetical Lineweaver–Burk plot. As extensively described elsewhere (Cook and Cleland, 2007, Cornish-Bowden, 2012 and Segal, 1975), the Michaelis–Menten equation (Eq. (2)) can be linearized as shown in Eq.

Leakage of joint fluid into the sheath of a joint nerve branch, w

Leakage of joint fluid into the sheath of a joint nerve branch, which is subsequently pumped into the nerve sheath of a main nerve, is the pathophysiological substrate of intraneural ganglia [36] and [37]. Ultrasonography characteristically shows multiple

well-defined anechoic cysts within the continuity of the nerve, which are filled with joint fluid and displace the nerve fascicles (Fig. 6). Most ganglia arise from the superior tibio-fibular joint involving either the common peroneal or the tibial nerve, but they may also affect the tibial nerve at the ankle or the ulnar nerve at the elbow. A recent study by Visser Selleck TSA HDAC [36] has demonstrated that intraneural ganglia account for approximately 18% of peroneal mononeuropathies at the fibular head, which underlines that ultrasonography is www.selleckchem.com/products/torin-1.html a valuable examination technique that is complementary to electrodiagnostic studies in these patients. In summary, ultrasonography of peripheral nerves is a valuable adjunctive modality in the clinical neurophysiology laboratory. Information on pathologic changes

in nerve structure and in the adjacent tissue in conjunction with information obtained by electrodiagnostic studies on the severity and chronicity of a disturbed nerve function and on the underlying demyelinating or axonal process may provide a more comprehensive picture of peripheral nerve diseases

compared to what can be provided by each modality alone [38]. Furthermore, information on nerve structure are often indispensable for clinical decision Edoxaban making. With respect to that purpose, ultrasonography is superior to magnetic resonance imaging in several aspects including not only costs, accessibility, portability, speed of examination, and patient comfort, but also technical properties such as spatial resolution and the ability to perform dynamic examinations during limb movements. Ultrasonography offers neuromuscular clinicians a unique opportunity to conduct both complementary examination modalities by themselves without referring patients to another laboratory. Currently, however, only a few neuromuscular clinicians are familiar with neuromuscular ultrasound. More efforts are necessary toward establishing examination guidelines and launching educational programs with appropriate certification by relevant accrediting societies to achieve a more widespread use of ultrasonography in clinical neurophysiology laboratories. The author declares that there is no actual or potential conflict of interest including any financial, personal or other relationships with other people or organizations within three years of beginning the submitted work that could inappropriately influence, or be perceived to influence, his work.

2) Both CTmax and heat coma values were significantly different

2). Both CTmax and heat coma values were significantly different between species and were progressively greater from C. antarcticus (30.1 and 31.8 °C), through M. arctica (31.7 and 34.6 °C), to A. antarcticus (34.1 and 36.9 °C) (P < 0.05 Tukey’s multiple range test, variances not equal). A one

month acclimation at −2 °C significantly reduced CTmax and heat coma temperatures compared to individuals maintained at +4 °C in all species (Fig. 2, P < 0.05 Kruskal–Wallis test). A two week acclimation at +9 °C also led to lower (or unchanged – C. antarcticus) CTmax and heat coma temperatures, though this was only significant for the heat coma temperature of A. antarcticus (P < 0.05 Kruskal–Wallis test). Summer acclimatised individuals of C. antarcticus exhibited significantly lower CTmax and heat coma temperatures Ibrutinib than individuals acclimated at either −2 °C or +4 °C, while summer acclimatised individuals of A. antarcticus only showed significantly lower CTmax and heat coma temperatures than individuals maintained at +4 °C. Across all temperatures between −4 and 20 °C, both collembolan species were significantly more active and travelled a greater distance than the mite (P < 0.05 Kruskal–Wallis

test, 4 °C acclimation, Fig. 3). In all species KU-57788 previously acclimated at +4 °C, movement increased with temperature up to 25 °C (except at 9 °C in M. arctica), before decreasing again at temperatures ⩾30 °C. Following an acclimation period at −2 °C (0 °C for M. arctica), there was no significant difference in locomotion at temperatures ⩽0 °C, except for M. arctica, in which movement was significantly greater at −4 °C (P < 0.05 Tukey’s multiple range test, variances not equal) ( Fig. 3). At 15 and 20 °C, movement was most rapid in C. antarcticus acclimated at −2 °C, as compared with the two other acclimation groups. The movement of M. arctica, acclimated at 0 °C, was also more rapid at 20 °C. Individuals of both collembolan species given an acclimation period at +9 °C exhibited considerably

slower movement at temperatures above +4 °C than individuals maintained at +4 °C. In contrast, movement was greater across all temperatures between 0 and 25 °C in +9 °C acclimated individuals mafosfamide of A. antarcticus. There were no significant differences in the SCPs of the three species when maintained at +4 °C (Table 1, P < 0.05 Kruskal–Wallis test). Alaskozetes antarcticus was the only species to show a bimodal distribution. In all three species, the SCPs of individuals acclimated at −2 °C for one month, and summer acclimatised individuals of C. antarcticus and A. antarcticus, were significantly lower than those of individuals maintained at +4 °C (P < 0.05 Kruskal–Wallis test). Conversely, the SCP of individuals after a +9°C acclimation period was not significantly different to those maintained at +4 °C (P > 0.05 Kruskal–Wallis test). Summer acclimatised individuals of C. antarcticus also had significantly lower SCPs than individuals acclimated at −2 °C (P < 0.

Briefly, blood samples were drawn by antecubital venipuncture whi

Briefly, blood samples were drawn by antecubital venipuncture while the individuals, who had not been fasting prior to any invasive procedure, were seated. The samples were collected in an 8.5-cc

Serum Separator Vacutainer Tube (BD Diagnostics, Plymouth, UK) and maximally within 4 h at room temperature were centrifuged at 1000 × g for 10 min. Serum samples were then distributed into sterile 500-μL barcode labeled polypropylene aliquots (TrakMate; Matrix TechCorp.) and stored at −80 °C. All serum samples were thawed on ice once and randomly placed in barcode labeled PI3K inhibitor racks in an 8-channel Hamilton STAR® pipetting robot (Hamilton) for automated aliquotting into 60-μL daughter tubes. The aliquots were stored in 96-tubes racks at −80 °C until further sample processing. Samples from the calibration and the validation set were distributed over three 96-tubes racks as following: one full 96-tube rack for both the calibration and validation set and one partially filled 96-tube rack with 63 samples from the calibration set and 18 samples from the validation set. Identical

processing steps were followed for the two sample sets. The isolation of peptides from human serum was performed using RPC18-functionalized MBs as previously described [27]. In short, RPC18-MBs were first activated by a three-step washing with a 0.1% TFA solution. Then, for each sample 5 μL of serum was added to the activated beads and incubated for 5 min at room selleck compound temperature. The beads were washed again three times with 0.1% TFA and peptides were eluted with a 1:1 mixture of water and acetonitrile. Two microliters of each

(stabilized) eluate were mixed with 10 μL of an α-cyano-4-hydroxycinnamic acid MALDI matrix solution in a 384-well PCR plate. Then, 1 μL of this mixture was spotted in quadruplicate onto a 600 μm Anchor-Chip™ MALDI-target plate (Bruker Daltonics). The so-called Palbociclib in vivo RPC18 eluates from the calibration and the validation set were spotted onto three 384-spots MALDI-target plate as following: 96 eluates from the calibration set and 96 eluates from the validation set were spotted in quadruplicate onto two distinct MALDI-target plates; the remaining eluates from the two sets were spotted in quadruplicate onto the same MALDI-target plate. This SPE- and MALDI-spotting procedure requires approximately 3 h per plate of 96 samples. MALDI-FTICR experiments were performed on a Bruker 15 tesla solariX™ FTICR mass spectrometer equipped with a novel CombiSource (Bruker Daltonics). The MALDI-FTICR system was controlled by Compass solariXcontrol software and equipped with a Bruker Smartbeam-II™ laser system that operated at a frequency of 200 Hz. The ‘medium’ predefined shot pattern was used for the irradiation.