As described by Assiry et al. (2003) one of the main reactions influencing degradation is the electrolysis of water, which yields hydrogen at the cathode and oxygen at the anode. Since

alternating current is used in the system both reactions occur at each electrode. equation(4) Cathode:2H+(aq)+2e−→H2(g) equation(5) Anode:2H2O(l)→O2(g)+4H+(aq)+4e− equation(6) Overall:2H2O(l)→2H2(g)+O2(g) According to the authors, the molecular oxygen generated by water electrolysis causes additional oxidation of the ascorbic acid. The presence of molecular oxygen in the system presented in this work could be related to the observed anthocyanin degradation. Another important reaction, also described by Assiry et al. (2003), is electrode corrosion. These reactions may happen in the ohmic heating systems either by direct metal oxidation or by electrochemical generation of corroding chemicals. The direct selleck inhibitor metal oxidations yields hydrogen and metal ions, these ions migrate into the medium

and can be oxidized and undergo other secondary reactions. In an agitated system, like the apparatus used in this work, the products of the previously described reactions could have dispersed in the pulp, where further reactions may have occurred, enhancing degradation. The frequency of electrochemical reactions is greater when higher voltages are used, as observed in the experiments of Içier and Ilicali IAP inhibitor (2005), Palaniappan and Sastry (1991) and Qihua, Jindal, and Van Winden (1993). In the last mentioned work, bubbles were produced during the ohmic heating of orange juice as a result of electrochemical reactions. Like ascorbic acid, anthocyanins are effective antioxidants and therefore oxidize easily (Skrede et al., 2000).

The unsaturated nature of anthocyanins makes them prone to attack by molecular oxygen; consequently, anthocyanins are likely to undergo similar chemical reactions, and these reactions may explain the observed behavior. When metallic electrodes are used, electrochemical reactions must always 4��8C be taken into account when frequencies between 50 and 60 Hz are used (Ruan et al., 2002). In the present study, it was possible to observe the deposition of black materials on the electrodes during the use of the experimental apparatus, and the Pt-100 m lost their black color due to the dissociation of the nickel–phosphorous alloy coating. According to the literature, the use of inert materials for the electrodes and the use of high frequencies are able to prevent electrochemical reactions (Içier & Ilicali, 2005). These effects can be observed in the study of Jun, Sastry, and Samaranayake (2007), who showed that retort pouches used with stainless steel electrodes and high frequencies can minimize bubble formation.

In the in vitro study, the conjugate presented a great cytolytic activity in DU 145 prostate cancer cells and SK-OV ovarian cancer cells that exhibited high MMP-2 activity. Besides, the conjugate showed low cytotoxicity in normal cells with selleck chemical low MMP-2 activity in vitro. In vivo, the tumors injected with the complex melittin/avidin were maintained with a smaller size

comparing to non-treated tumors, indicating the great potential of this treatment in the fight against cancer. Ling et al. (2004) built a recombinant adenovirus carrying the melittin gene and α-fetoprotein (AFP) promoter (Ad-rAFP-Mel). It has been shown that the melittin mRNA was transcribed in HepG2 hepatocellular carcinoma cells transduced by AdrAFP-Mel. The tumorigenicity rates of hepatocarcinoma cells transfected with Ad-rAFP-Mel were lower comparing with non-transfected cells. A significant antineoplastic effect was detected in the transplanted tumor in nude mice after an intratumoral injection

of Ad-rAFP-Mel. Ling et al. (2005) also reported lower tumorigenicity rates of hepatocarcinoma cells transfected with Ad-rAFP-Mel. A significant antineoplastic effect was detected on the transplanted tumor in nude mice after an intratumoral injection of Ad-rAFP-Mel. Li et al. (2006) further showed that an AdrAFP-Mel infection markedly induces cellular apoptosis, and Fas expression on Bel-7402 cells. They suggested this to be a possible molecular mechanism KU-57788 solubility dmso for the antitumorigenecity of AdrAFP-Mel even though more studies will be needed. In an in vivo study, Orsolic et al. (2003) showed that, when intravenously injected, BV significantly Cediranib (AZD2171) inhibited mammary carcinoma metastasis (P < 0.001)

in mice injected also intravenously with this type of tumor, when compared to control mice. However, when the venom was subcutaneously administered, no differences in metastasis formation were observed. The tumor also decreased in size when the venom was administered intratumorally, and mice survived longer than control, indicating that the in vivo venom action depends on how the venom is injected. Jang et al. (2003) studied the effects of BV in NCI-H1299 lung cancer cells and verified that cells treated with 10 μg/ml of venom for 24 h exhibited morphological changes typical of apoptotic cells, which was confirmed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, DAPI staining assay and DNA fragmentation detected via agarose electrophoresis. Furthermore, flow cytometric analyses showed an accumulation of cells in the sub G1 phase of cell cycle in treated cells compared to control. It was also demonstrated that BV treatment resulted in an increase in the expression of Bax, a pro-apoptotic protein, and a decrease in the expression of Bcl-2, a protein that heterodimerizes with Bax, suppressing cell death.

They are often violated in published work, however, so apparently they are not perceived as obvious. The essential point is that an experiment should be capable of supplying the information that the experimenter is seeking to extract. The necessary design, therefore, must depend on the context in which the experiment is being used. If the aim is to obtain kinetic parameters to be used for elucidating an enzyme mechanism, the conditions need to be varied in ranges in which the results

vary with the parameter of interest. If the aim is to understand the physiological role of an enzyme it needs to be studied in conditions that do not depart more than necessary from physiological conditions. All this is simply common sense, but it is useful to consider it in a little Caspase inhibitor clinical trial more detail. This is a point that arises when there are two or more independent variables—two different substrate concentrations, for example, or a substrate and an click here inhibitor concentration. Put in words it is indeed obvious: if two variables are not independent then they are not independent! However, in practice it may not be obvious without an understanding of what independence means. This is easy to define for a linear regression model: it is sufficient to require that two independent variables x1x1 and x2x2 must not satisfy any linear equation

x2=a+bx1x2=a+bx1, where a and b are any constants. It is also easy to illustrate the consequences of violating this requirement in a linear regression. Virtually none of the Branched chain aminotransferase equations considered in enzyme kinetics lead to linear models if properly analysed, 1 but in practice it is not difficult to ensure that the independent variables are indeed independent even in a non-linear regression: in essence, it means that knowledge of the values of one independent variable must not allow the values

of another to be calculated. In the simplest case, concentrations must not be varied in constant ratio, or with a constant sum. This does not of course exclude the possibility that one may want to remove the independence between two or more variables. For example, the method of Yagi and Ozawa (1960) for analysing multiple inhibition involves using linear combinations of the concentrations of two or more inhibitors, and that proposed much more recently by Cortés et al. (2001) for assessing whether two competing substrates bind at the same site involves linear combinations of the two substrate concentrations. In these sorts of experiments one is deliberately suppressing differences between the effects of the two variables in order to shine more light on some effect of the two together, and as long as this is understood there is no objection to the use of linear combinations of concentrations.

Semantic effects on naming must therefore arise outside the normal naming process. For example, one might credibly ask whether the effects we observed could be “post-lexical”, arising not from the computation

of the phonological code but from subsequent learn more decision or integration processes. Such post-lexical processes are an important component of reading comprehension, as in the interpretation of multi-word sequences (Desai et al., 2010 and Humphries et al., 2006) and the integration of words with prior linguistic context (Hagoort, 2008). However, the naming task used in the present study makes no demand on decision or integration processes and is notably insensitive to such effects, in contrast to tasks such as lexical decision (Balota et al., 1991 and Seidenberg et al., 1984). In addition, although canonical semantic effects such as the N400 occur relatively late in the time course of word recognition, effects of semantic variables such as semantic coherence (the number of contexts in which a word occurs) have been detected 160 ms post word onset (Hauk et al., 2006 and Pulvermüller et al., 2009). This

timeframe corresponds to early stages buy ABT-888 of word recognition and reading aloud (Barber & Kutas, 2007), demonstrating that semantic effects are not restricted to later integration or decision-related processes. The cognitive loci of semantic effects are discussed further below. In short, the dual-route framework does not incorporate a role for semantics in the generation of pronunciations. Therefore it provides no explanation of why individuals vary in their use of semantic information during reading aloud, nor any hypotheses for what the neural basis of this variation might be. It is for these reasons that we feel the triangle framework is most useful for interpreting the current results. However, we should be clear that the goal of the current study was not to adjudicate between the triangle and dual-route models, but rather to investigate the neural basis of individual differences in the use of semantics in skilled PLEKHB2 reading aloud. The triangle model framework will be used for two purposes: to ground the interpretation

of the functions of the areas and pathways seen in the neuroimaging results, and to understand the behavioral and neuroanatomical individual differences associated with the use of semantics in reading aloud. This analysis yields a closer integration of the computational framework and neurobiological data, but also reveals limitations of existing models and questions concerning factors that determine the “division of labor” between components of the reading system. The extent to which imageability affected performance in reading aloud predicted ITS-pMTG pathway volume. Involvement of the ITS region in semantics is suggested by several converging findings (Cattinelli et al., 2013, Rohrer et al., 2009, Whitney et al., 2011 and Woollams et al.

After 60 min of reaction at 37 °C, release of Pi was colorimetrically measured as previously described (Fiske and Subbarow, 1925). Yolk granule suspensions were obtained by gently rupturing of 24-h-old eggs in 0.4 M sucrose, 10 mM Hepes pH 7.2. Samples

click here were washed (1 min, 10,000g, room temperature centrifugation), and fixed at room temperature for 30 min in 0.4 M sucrose, 10 mM Hepes pH 7.2, 0.5% glutaraldehyde, 0.5% formaldehyde. After washing in 0.4 M sucrose, 10 mM Hepes pH 7.2, samples were resuspended and incubated for 1 h at 37 °C in acid phosphatase reaction medium (1 mM sodium β-glycerophosphate, 2 mM CeCl3, 0.1 M sucrose, 0.1 M sodium acetate pH 4.0) ( Hulstaert et al., 1983). Controls were carried out without the substrate or in the presence of 10 mM Na+ K+ tartrate. Samples were washed twice in 0.1 M sodium acetate pH 4.0, once in 0.1 M sodium cacodylate pH 7.2 and posteriorly fixed for AZD6244 datasheet 2 h at room temperature by 2.5% glutaraldehyde, 4% formaldehyde, 0.1 M sodium cacodylate pH 7.2. Samples were then washed in cacodylate buffer, post-fixed in 1% OsO4 for 1 h at room temperature, dehydrated in ethanol series and embedded in a Polybed 812 resin. Ultrathin sections were observed in a JEOL 1200 EX transmission electron microscope, operating

at 80 kV. For X-ray microanalysis, X-rays were collected for 150 s using a Si (Li) detector with a Norvar window in a 0–10 keV energy range with a resolution of 10 eV/channel. Analysis was performed using a Noran Voyager III analyzer. Freshly-laid eggs were homogenized in 20 mM Hepes pH 7.5 and centrifuged twice for 10 min at 18,000g at 4 °C. Supernatants were centrifuged at 10,000g for 2 h at 4 °C in a Millipore Ultrafree-MC-5 centrifugal filter unit and retained samples were resuspended in 20 mM Hepes pH 7.5, and labeled “yolk protein”. Following, 40 μg of “yolk protein” was incubated

at 37 °C in a reaction medium (P8340 protease inhibitor cocktail, 2.5 mM DTT, 2.5 mM EDTA, 25 mM sodium acetate pH 4.0) containing 0.32 μg agAP protein. When specified, 10 mM Na+ K+ tartrate was used as agAP inhibitor. Following, 12.5% Sulfite dehydrogenase SDS–PAGE was performed and the proteins were transferred to a nitrocellulose membrane that was blocked for 90 min with blocking buffer (0.05% TBS-Tween 20, 3% BSA). The membrane was then incubated overnight in blocking buffer containing 1:1000 PY-99 (raised against phosphotyrosine). Membrane was washed and revealed using a SuperSignal West Pico (Pierce) after incubation of 1:2000 anti-mouse peroxidase-conjugated IgG. All incubation steps were performed at room temperature. PolyP detection was performed as described (Gomes et al., 2008). Briefly, yolk granule suspensions were obtained by gently rupturing of 24-h-old eggs in 20 mM Hepes pH 7.2. Samples were washed (1 min, 10,000 g, room temperature) and incubated in 20 mM Hepes pH 7.2, 50 μg/mL DAPI for 20 min at room temperature.

, 2007 and Karlson et al., 2008). PTJC=Prediction of Tender Joint Count=−26.72+3.243∗[YKL-40]1/10−11.97*[EGF]1/10+15.72∗[IL-6]1/10+0.4594∗[Leptin]1/10+3.881∗[SAA]1/10+0.7388∗[TNF-RI]1/10−0.2557∗[VCAM-1]1/10+0.7003∗[VEGF-A]1/10 PSJC=Prediction of Swollen Joint Count=−26.63+3.232∗[YKL-40]1/10−11.93∗[EGF]1/10+15.67∗[IL-6]1/10+0.4578∗[Leptin]1/10+3.868∗[SAA]1/10+0.7363∗[TNF-RI]1/10−0.2548∗[VCAM-1]1/10+0.6979∗[VEGF-A]1/10

BMN 673 ic50 PPGS=Prediction of Patient Global Score=−13.489+5.474∗[IL-6]1/10+0.486∗[SAA]1/10+2.246∗[MMP-1]1/10+1.684∗[Leptin]1/10+4.14∗[TNF-RI]1/10+2.292∗[VEGF-A]1/10–1.898∗[EGF]1/10+0.028∗[MMP-3]1/10–2.892∗[VCAM-1]1/10–0.506∗[Resistin]1/10 MBDA score=round(max(min((.56∗sqrt(max(PTJC,0))+.28∗sqrt(max(PSJC,0))+.14∗PPGS+.36∗log(CRP/10^6+1))∗10.53+1,100),1))MBDA score=roundmax(min((.56∗sqrt(max(PTJC,0))+.28∗sqrt(max(PSJC,0))+.14∗PPGS+.36∗log(CRP/10^6+1))∗10.53+1,100),1)

All concentration values except that of CRP are X1/10 transformed prior to use in the algorithm. MBDA algorithm scores are integers from 1 to 100, with disease activity thresholds designed to be equivalent Everolimus order to thresholds from DAS28CRP: • MBDA algorithm scores ≤ 29 are considered low disease activity. All autoantibody assays exhibited less than 10% difference (median difference) between the two sample types (Table 3), well within the Food and Drug Administration suggested specification at ± 15% for accuracy (FDA, 2001). Phosphoprotein phosphatase All analyses for autoantibodies were calculated on raw signals in antibody biomarker measurements. An additional more stringent analysis compared the correlation coefficient and slope of linear regression. In comparison of plasma and serum matched sample sets, the correlation was 0.99 (0.98 to 1.00) with a slope of approximately

1.00, indicating little or no difference in quantitation of autoantibody signals in serum vs. plasma samples. For protein biomarkers of matched plasma and serum samples, only 67% of the biomarkers were highly correlated achieving correlation coefficients of 0.95 (range 0.33–1.00) (Table 3). The protein concentrations had a systematic shift with the slope of most markers being less than 1.00, indicating serum concentrations were measured higher for most biomarkers. The plasma EGF concentrations were not correlated with matched serum EGF concentrations (correlation coefficient of 0.33). As shown in Fig. 1A, 5 out of 12 protein biomarkers (VCAM-1, EGF, VEGF-A, MMP1 and resistin) had shifts > 15% in the median % difference in concentration across the 32 patient samples. Aside from leptin and MMP-1, median protein concentrations in plasma were lower than those in serum. While the median change for MMP-1 showed significantly greater concentrations in plasma over serum (Fig. 1A), the individual subjects in this study provided mixed results, with 12 subjects’ plasma showing lower MMP-1 concentrations and 20 subjects with greater MMP-1 concentrations.

The 95% CIs were constructed around the observed response rates and for the differences in response rates between treatment groups. Patient-reported fatigue and impairment in productivity, daily activities, and missed work time were analyzed as change from baseline selleck inhibitor using a piecewise linear model comparing the area under the score–time curve from baseline with week 60, allowing slopes to change over time for each treatment arm. These

end points were prespecified in the statistical analysis plan in the order presented as part of a closed testing procedure to address multiple testing of secondary end points. All statistical analyses were performed using SAS version 9.1 (SAS Institute, Inc, Cary, NC). A total of 462 patients were screened; of these, 394 were randomized and 393 were treated (260 in the simeprevir/PR group and 133 in the placebo/PR group) (Supplementary Figure 2). At the time of this primary analysis, all patients

had reached the time point at which the primary end point (SVR12) was assessed (ie, week 60), or had discontinued earlier. In addition, Lapatinib research buy 184 patients (46.8%) had completed the final week 72 visit, and 24 (6.1%) had discontinued the study prematurely. The main reasons for study discontinuation were withdrawal of consent (14 patients; 3.6%) and loss to follow-up evaluation (8 patients; 2.0%). Most (93.1%) patients in the simeprevir/PR group completed their assigned treatment regimen (compared with 25.6% in the placebo/PR group). The proportion of patients who discontinued simeprevir/placebo intake early was 3.5% and 72.2% in

the simeprevir/PR and placebo/PR groups, respectively. The main reason for discontinuation was meeting the week 4 virologic stopping rule for simeprevir or placebo in both arms, with a large proportion of patients learn more in the placebo group (69.9%) stopping placebo at week 4. The proportion of patients who completed PR treatment was 93.5% in the simeprevir/PR group (24 or 48 weeks) and 72.2% in the placebo/PR group (48 weeks). Baseline demographic and disease characteristics were comparable between groups (Table 1; Supplementary Results section). The median times (in months) between the end of previous (Peg)IFN-based therapy and the start of treatment in this study were as follows: 31.0 (4; 141) and 31.0 (5; 115) for the simeprevir and placebo groups. In the simeprevir/PR arm, an SVR12 rate of 79.

However, the number of PCs and RBCs transfused was similar in the two study arms, and the authors raised the question of whether the CCI is a reliable surrogate marker for bleeding risk assessment.

As shown by the studies discussed above, the results of the published clinical studies should be interpreted with caution, and their characteristics and possible biases should be taken into account. Results obtained with one method cannot be extrapolated to those obtained by other methods. In the first published meta-analysis that included the HOVON trial, Vamvkas concluded that there was a clinically significant increase in mild and moderate bleeding complications in the arm receiving treated-platelets [85]. However, this meta-analysis Cabozantinib ic50 contained a serious methodological bias: it combined the results of clinical studies of amotosalem/UVA with the results of a clinical study of riboflavin/broad spectrum UV. In a second meta-analysis, which was recently published by Cid et al., although the CCIs were lower after INTERCEPT, the hemostatic

efficacy of INTERCEPT-treated PCs was maintained. These findings support the results of previously published hemovigilance data, which did not show an increase in the number of PC transfusions after INTERCEPT [86]. The beneficial effects of INTERCEPT-treated platelets have been clearly demonstrated. Indeed, they reach beyond the original scope: in addition to the reduction in infectious risk, INTERCEPT-treated platelets obviate the need for γ-inactivation for GvHD prophylaxis and extend the maximum shelf life of platelets from 5 to 7 days. Furthermore, a reduction

in the transfusion MEK phosphorylation reaction rate has been observed, due either to partial plasma substitution Loperamide by additive solution or to a specific PI effect. Although platelet recovery, as measured by CCI or survival studies with radiolabeled platelets, is lower after PI treatment, the hemostatic efficacy, as measured by clinical outcomes, is maintained. The results of prospective clinical trials have been confirmed by retrospective hemovigilance data. However, the heterogeneity of these clinical trials complicates their comparison. At the laboratory level, PI-treated platelets seem to present an increased activation status, and moderate changes at the level of mitochondrial metabolism are expressed in increased metabolic parameters; however, the results are discordant among studies. These modifications might explain the reduced survival and decreased recirculation level of PI-treated platelets, although the increased activation status of PI-treated platelets does not lead to a decrease in hemostatic efficacy. Activated fibrinogen receptor expression appears to be increased after PI, perhaps through a direct effect of PI on this integrin. These data relate mainly to the amotosalen/UVA technique and, to a lesser extent, to the riboflavin/UV method.

In 2010, the available literature was insufficient evidence for the American Gastroenterological Association to make recommendations for or against the use of thiopurines as potential chemopreventive agents.36 Selleckchem Talazoparib However, recent clinical studies have provided sufficient evidence to reconsider

the potential for 6-MP and AZA to reduce the risk of colitis-associated dysplasia and CRC in patients with IBD. Two large population-based cohorts, similar to prior studies, had different results. In a Dutch cohort of 2578 patients with IBD, van Schaik and colleagues33 reported that 28 patients (1%) developed HGD or CRC during 16,289 person-years of follow-up. Two of 28 patients (7%) were on thiopurines alone and 1 patient (of 28, 4%) was on a thiopurine plus 5-ASA. Thiopurine use was associated with a significantly decreased risk of developing HGD or CRC with an adjusted hazard PD-166866 ic50 ratio (HR) of 0.10 (95% CI 0.01–0.75). However, Pasternak and colleagues37 found no protective benefit in a Danish cohort of 45,986 IBD patients, of which 11% were on AZA (adjusted relative

risk [RR] = 1.00; 95% CI 0.61–1.63). In 2013, the first prospective study of the epidemiology of colorectal HGD and cancer in IBD in the thiopurine era was published by Beaugerie and colleagues.38 The results of the CESAME (Cancers Et Surrisque Associé aux Maladies Inflammatoires Intestinales ID-8 En France) trial, a French nationwide observational cohort of 19,486 patients with

IBD designed in the early 2000s to assess the risks of any cancer or HGD in IBD patients, found that 57 (0.3%) patients developed HGD or CRC during the follow-up period (37 CRC, 20 colorectal HGD). In patients with long-standing, extensive colitis, defined as disease duration of at least 10 years and extent of at least 50% of the colon, the multivariate adjusted HR for colorectal HGD and CRC was 0.28 for those who received thiopurines (95% CI 0.1–0.9; P = .03). In the study of inflammation risk by Rubin and colleagues,5 multivariate analysis identified thiopurine exposure as a significant predictive factor (adjusted OR 0.25; 95% CI 0.08–0.74). This finding, after controlling for degree of inflammation, was one of the strongest lines of evidence to date. A meta-analysis pooling of 19 studies (9 case-control and 10 cohort studies), while acknowledging high heterogeneity among studies (I2 = 68.0%, P<.001), reported that the use of thiopurine was associated with a statistically significant decreased incidence of CRC or dysplasia (HGD and LGD) with a pooled RR of 0.71 (95% CI 0.54–0.94; P = .017), even after adjustment for duration and extent of the disease. 39 In the thiopurine-treated patients, the RR of HGD and CRC was 0.72 (95% CI 0.50–1.03; P = .070) and 0.70 for CRC (95% CI 0.46–1.09; P = .111).

2%), intestinal schistosomiasis 4.8% (95% CI 1.0–13.3%) vs 8.5% (95% CI 2.8–18.7%) and hookworm 20.6% (95% CI 11.5–32.7%) vs 20.3% (95% CI 11.0-32.8%). Again there was no statistical imbalance between prevalence by Fisher’s χ2 test between inside and outside the circle for either mothers or children, although it is of note that both prevalence of intestinal schistosomiasis and malaria in mothers declined slightly outside this circle.

Vincristine The results of the scan statistic revealed no significant high or low prevalence clusters for malaria. However, a low prevalence cluster was identified for hookworm (approximately at 0.31°N, 33.5 °E, radius 0.20 km) where there were no cases found in an area expected to have approximately seven cases (P=0.072). While we lacked

power to detect significant clustering for schistosomiasis, the most likely cluster identified was for a high prevalence region (approximately at 0.31°N, 33.5°E, radius 0.08 km) where there were eight cases in an area expected to have three (P=0.81). No significant clustering was found for persons with two or more types of parasite infection. To our knowledge this is the first report of using GPS-data loggers to record the spatial distribution of households of study participants within a point-prevalence survey. Whilst it is outside the immediate remit of this paper MYO10 to conduct a detailed multivariate analysis of our data with geospatial Forskolin concentration models, Figure 2 and Figure 3 adequately demonstrate the potential of this methodology to capture the location of each household using small GPS units. Annotating these households by infection status of occupants can very quickly reveal occurrences of disease focality, or proximity to likely infectious sources. The data logging principle has been explored previously using larger units housed inside a wearable waistcoat for

mapping the outdoor activities patterns of people tending rice paddies and more recently with I-GotU units for tracking human movements in relation to exposure to infection from dengue viruses.21 and 24 Using the I-GotU to identify the exact position of each household has, in this instance, revealed that the micro-patterning of diseases within Bukoba was not immediately ‘clumped’ which is reassuring that the initial point-prevalence statistic from the 126 households did not contain cryptic micro-patterns, such that, the 63 households that were later geotagged and annotated for each of the three diseases examined were also broadly representative.