In a previous experiment it was noticed a significant increase of

In a previous experiment it was noticed a significant increase of the hemagglutination activity upon leaf injury (data will be published elsewhere). After this, the leaves were powdered in the presence of liquid nitrogen and stored at −80 °C until required. DEAE-cellulose column was obtained from Whatman International

Ltd., Maidstone, England; Phenyl-Sepharose 6-Fast Flow column was obtained from GE Healthcare, Uppsala, Sweden. Morphine was purchased from Sigma Aldrich Chemical (Saint Louis, MO, USA). selleck chemicals The other chemicals were all of analytical grade and obtained from local suppliers. The soluble proteins were extracted from the leaf powder with three volumes of 25 mM Tris–HCl, pH 7.5, supplemented with 3% (w/v) polyvinylpolypyrrolidone (PVPP) and 5 mM ascorbic acid, for 2 h at 4 °C, under gentle shaking. After filtration through nylon cloth, the filtrate was centrifuged at 10,000 × g for 30 min, at 4 °C, and the supernatant (crude extract) recovered. The crude extract was precipitated with ammonium sulfate at 30% saturation (176 g/L) and the suspension maintained at 4 °C for 12 h. The precipitate obtained (Fraction 0–30%, shortly F030) after centrifugation (10,000 × g, Selleckchem CP 868596 40 min, 4 °C) was dialyzed exhaustively against Milli-Q grade water, lyophilized, and suspended in 25 mM Tris–HCl, pH 7.5. After centrifugation (10,000 × g, 20 min, 4 °C), the fraction

F030 was submitted to ion-exchange chromatography on a DEAE-cellulose column equilibrated with 25 mM Tris–HCl, pH 7.5. The through fraction was eluted from the column with the equilibrating buffer. The retained material was eluted with 25 mM Tris–HCl, pH 7.5, containing 200 mM NaCl, at a flow rate of 1 mL/min, dialyzed exhaustively against water and lyophilized. Next, it was suspended in 25 mM Verteporfin Tris–HCl, pH 7.5, containing 420 mM of ammonium sulfate, centrifuged (10,000 × g, 20 min, 4 °C), and the supernatant obtained chromatographed on a Phenyl-Sepharose 6-Fast Flow column, equilibrated with the above buffer.

The protein fraction obtained after elution with 25 mM Tris-HCl, pH 7.5, containing 100 mM of ammonium sulfate, at a flow rate of 1 mL/min, was dialyzed against Milli-Q grade water and lyophilized. This material represented the lectin-enriched fraction (LEF) that was characterized and used to assess toxicity. It was determined as previously described (Bradford, 1976). Absorbance at 280 nm was also used to monitor protein elution profiles during chromatographies. Protein fractions were analyzed by polyacrylamide gel electrophoresis (15% running gel, 3.5% stacking gel) (Laemmli, 1970). The samples were solubilized in 125 mM Tris–HCl buffer, pH 6.8, containing 2.6% (w/v) SDS, 0.5 mM EGTA, 0.5 mM EDTA, 12.6% (w/v) glycerol. Gels were stained with silver (Blum et al., 1986).

Indirect stakeholder involvement covers contributions to the fram

Indirect stakeholder involvement covers contributions to the framing of the modelling endeavour, model evaluation and model use. Various sub-forms of indirect involvement are conceivable. Stakeholders can be invited to review the design of the model, a process corresponding

to the extended peer review concept. Stakeholders can also be asked to provide input to model use in form of scenarios (in terms of policy or management options), or in form of critical reflections over the causal logic of these inputs. The appropriate stage(s) for stakeholder input in the modelling process need to be identified at an early stage [21]. To stimulate the feeling of ownership and to increase legitimacy and effectiveness, KU-60019 stakeholders should be involved from the very first, the problem-framing, step. Drakeford et al. [25] and Dreyer et al. [18] carried out a literature review of participatory modelling in natural resource governance. The synopsis of the results of this review offers, in short form, practical implementation assistance to such participatory

exercises [29]. Drawing on main analytical distinctions provided by the literature screened, it sets out different purposes envisaged, specifies different modelling phases at which stakeholders could be involved [21], and points out how the timing of participation is linked to the degree to which stakeholders can influence model-based

knowledge ABT-199 clinical trial output. One basic design principle of participatory processes is clarity of Reverse transcriptase purpose for all participants [14, p. 228]. A participatory process should be designed with a clear purpose in mind of both, modelling and deliberation, and sharing this understanding with all participants. Dreyer and Renn [29] highlight four purposes of participatory modelling in the context of natural resource governance [20], [22], [30], [31] and [32]: (A) Collective learning for consensus-building and/or conflict reduction; (B) knowledge incorporation and quality control for better management decisions; (C) higher levels of legitimacy of and compliance with management decisions; (D) advancing scientific understanding of potential and implementation requirements of participatory modelling. In fisheries, so far stakeholders have been involved in modelling activities only sporadically, mainly through research projects (e.g., EFIMAS, PRONE, GAP1), hence, with a focus on purpose D. The JAKFISH literature review found only few cases in Europe where participatory modelling aimed at directly supporting actual decision-making processes [33] and [34]. The characterization of uncertainties is an important element of participatory modelling approaches. Traditional characterizations based on quantifiable uncertainties [35] tend to ignore uncertainties that are not amenable to quantitative analyses.

2 μl/injection site) into the LPBN They were then deeply anaesth

2 μl/injection site) into the LPBN. They were then deeply anaesthetised with sodium thiopental (CRISTALIA, Itapira, SP, Brazil, 80 mg/kg of b.w.) and perfused transcardially with saline followed by 10% formalin. The brains were removed, fixed in 10% formalin, frozen, cut coronally into 60 μm sections and stained with Giemsa stain. Only animals with injections into the LPBN were considered for statistical analysis. The results are reported as means ± standard error of the mean (SEM). Statistical analysis was performed using two-way analysis of variance (ANOVA) with repeated measures followed by Student–Newman–Keuls post hoc tests to determine significant differences between

groups. IL-6 and TNF-α levels and alveolar bone loss were analysed by the Student AZD2281 price t-test. Differences were considered significant at P < 0.05. The software used to analyse the data was SigmaStat

Etoposide in vitro for Windows, version 2.03 from SPSS Inc. Alveolar bone analysis revealed that rats with periodontal disease had more bone loss than rats in the control group (1.29 ± 0.04 vs. CN group: 0.50 ± 0.02 mm, P < 0.001, Fig. 1), showing that the induction of periodontal disease was effective. There were no statistically significant differences between the ingestion (ml/24 h) of water and 0.3 M NaCl for both groups (control and PD rats) in any of the evaluation periods (3 and 16 days) after ligature-induced periodontal disease (Fig. 2). ANOVA showed significant differences among treatments and times for water intake (F(18,126) = 17.4; P < 0.001, Fig. 3C and D) and 0.3 M NaCl intake (F(18,126) = 5.4; P < 0.001, Fig. 3A and B) when fluid-replete rats had simultaneous access to water and 0.3 M NaCl. Compared with saline injections into the LPBN, the cumulative ingestion of 0.3 M NaCl and water significantly increased after injections of muscimol (0.5 nmol/0.2 μl at each site, n = 8) into the LPBN after 120 min until the end of the test in control and PD rats ( Fig. 3A and

C). Post Casein kinase 1 hoc tests showed that ligature-induced PD attenuated the effects of muscimol on water intake ( Fig. 3C and D) without changing 0.3 M NaCl intake ( Fig. 3A and B). ANOVA showed significant differences among treatments and times for water intake (F(18,126) = 6.9; P < 0.001, Fig. 4C and D) and 0.3 M NaCl intake (F(18,126) = 4.7; P < 0.001, Fig. 4A and B) when FURO + CAP-treated rats (control and PD) that received muscimol or saline in the LPBN had simultaneous access to water and 0.3 M NaCl. In control rats, the cumulative ingestion of 0.3 M NaCl after injections of muscimol (0.5 nmol/0.2 μl at each site, n = 8) into the LPBN was significantly different from ingestion after saline injections into the LPBN from 90 to 180 min of the test, with P values ranging from P < 0.05 at 90 min to P < 0.005 from 120 to 180 min (Newman–Keuls post hoc test) ( Fig. 4A and B).

A damaging effect

A damaging effect BKM120 supplier of alcohol on the liver is the production of defective mitochondria (Arai et al., 1984). Ethanol metabolism produces active oxidants inducing mitochondrial membrane depolarization. The mitochondrial permeability has been identified as a key step to apoptosis (Adachi and Ishii, 2002). Alcohol consumption has been shown to severely compromise mitochondrial protein synthesis (Cahill and Sykora, 2008). Alcohol intake may cause cellular unbalanced and cellular death. According to Lluis et al. (2003) and Lieber et al. (2007) alcohol ingestion resulted in lower mitochondrial GSH levels. Through

control of mitochondrial electron transport chain-generated oxidants, mitochondrial GSH modulates cell death and hence its regulation may be a key target to influence disease progression and drug-induced cell death (Fernandes-Checa and Kaplowitz, 2005). Direct DNA damage results from acetaldehyde, which can bind to DNA, inhibit DNA repairs systems and lead to the formation of carcinogenic exocyclic DNA etheno adducts. Chronic alcohol abuse interferes with methyl group transfer and may alter gene

expression (Seitz and Sticke, 2006). Panobinostat mw The capacity of mitochondria to oxidize acetaldehyde is significantly reduced in the presence of NAD-dehydrogenase substrates, with consequent high levels of acetaldehyde (Hasumura et al., 1975). Alcohol ingestion provokes metabolic modifications in hepatocytes, such

as reductions of fatty acid oxidation, glycogenesis and albumin (Thompson, 1978). The increase in acetate modifies fatty acid metabolism by inhibiting lipolysis, causing hepatic steatosis. Acetate is later released into blood plasma where it may be degraded, with the release of energy, or accumulated as fatty acids and cholesterol in extrahepatic tissues (Hirata and Hirata, 1991 and Mcgarry, 1992). In UCh rats the expression pattern of IGFR-I as the same of control rats. The literature Inositol monophosphatase 1 related few works about IGFR-I and palatine mucosa. Fergunson et al. (1992) described the differential expression of insulin-like growth factors I and II during mouse palate development. Brady et al. (2007) characterized the expression and function of IGF-I and IGF-II in oral squamous carcinoma and normal cell lines. Conflicting data are related about IGF-I and alcoholism in different tissues. It can be seen reduction on this growth protein (De La Monte et al., 2005) or increased expression of IGF-I and IGF-I receptors (Longato et al., 2008). No signs of metaplasia were observed agreeing with Bofetta et al. (1992), Summerlin et al. (1992) and Martinez et al. (2005) that mentioned that longer periods of alcohol ingestion may provokes such damages. Therefore, chronic ethanol ingestion altered the hard palate epithelium structure of rats UCh. This study was financially supported by CNPq/PIBIC and FAPESP.

thaliana (TAIR9, Swarbreck et al , 2008) and O sativa (Rice Geno

thaliana (TAIR9, Swarbreck et al., 2008) and O. sativa (Rice Genome Annotation Project v6.1, Ouyang

et al., 2007) via BLASTX (for a complete workflow see Fig. S4). Gene-expression profiles were analyzed by multivariate analysis to E7080 research buy identify similarities and differences of the entire transcriptomic response between species and treatment conditions. Transcription profiles of the eight libraries were normalized for library size and composition of expressed transcripts (Robinson and Oshlack, 2010). Groupings of expression profiles based on the biological coefficient of variation between library pairs were identified with multidimensional-scaling (MDS) using the R package “edgeR” v2.5.1 (Robinson et al., 2010). Identified groupings were tested by ANOSIM analysis (analysis of similarity, tests distances within vs. between groups) implemented in the R package “vegan” v2.0–3 (Oksanen et al., 2012). Multivariate analysis and subsequent expression analysis along with plotting functions were performed in R (R Development Core Team, 2008). Differential expression analysis was performed with the R package “edgeR”, which employs an overdispersed Poisson model (negative binomial) to account for technical and biological variability,

with the generalized linear model (GLM) functionality for multifactor experiments (Robinson et al., 2010 and McCarthy et al., 2012). Differentially expressed genes were determined for three data sets: 1) eight libraries including samples of both species, 2) four libraries this website of Z. marina and 3) four libraries of N. noltii. In all three data sets, the expression profiles were normalized for library size and composition of expressed transcripts ( Robinson and Oshlack,

2010). For the data set including both species (data set 1), the single factor species was fitted to the GLM to test for differential expression between both species consistent across treatments. In this case, all four libraries per species from the two different populations and treatments were used as biological replicates on the species level. For Z. marina alone L-NAME HCl (data set 2) the data were analyzed with GLM including the factors treatment and population (the factor population was suggested by the grouping of expression profiles; Fig. 1). Differential expression, with respect to heat treatment, was tested, while adjusting for the remaining factor. For N. noltii alone (data set 3) the factor “group identity” with three factor levels identified by MDS ( Fig. 1) was fitted to the GLM. Genes displaying differential expression between heat and control treatment in the northern population (two of the three groups, Fig. 1) were identified. In all three data sets, the biological replication as defined by the design of the respective GLM was used to calculate the tagwise dispersion, the overdispersion value in the negative binomial model ( Robinson et al., 2010 and McCarthy et al., 2012).

Information collected from the CRC patients was used to classify

Information collected from the CRC patients was used to classify the family risk status of their FDRs according to a modified version of the National Health and Medical Research Council’s risk categories [15]: Category 1. At or slightly above average risk: Index cases (ICs) with no first or second degree relatives diagnosed with bowel cancer and who were diagnosed themselves over age 55. FDRs that consented participated in a brief screening interview to assess trial Akt inhibitor eligibility. Those with a prior diagnosis of CRC, advanced adenoma or FAP, or Crohn’s disease, ulcerative colitis, or other inflammatory bowel disease were considered ineligible. Eligible FDRs completed a baseline

CATI comprising a series of modules

a subset of which are reported here. Socio-demographic find more questions: Items included age, gender, country of birth, postcode, marital status, level of education, employment status and whether they have private health cover. The relationship between the FDR and the IC was known from the IC interview. Awareness of family risk: FDRs were asked when they first became aware that having a family history of bowel cancer increases a person’s risk of developing bowel cancer (“less than a month ago”; “1 month to less than 12 months ago”; “12 months to less than 2 years ago”; “2 years to less than 5 years ago, 5 years or longer”; “Don’t know that family history increases for risk”), and were asked what first alerted them to this fact (“The letter I received from the Cancer Council”; “A member of my family was diagnosed with bowel cancer”; “Information from the TV, radio or newspaper”; “My doctor discussed the risk of bowel cancer with me”; “Other”; “Don’t know/Not sure”). Discussions with health professional: FDRs were asked whether a health professional had ever asked about their family history of bowel cancer, the type of health professional who asked (“GP”, “cancer specialist”, “genetic counsellor” or “other”), how long ago they were asked (“less than a month ago”;

“1 month to less than 12 months ago”; “12 months to less than 2 years ago”; “2 years to less than 5 years ago, 5 years or longer”; “Don’t know/ Not sure”) and how many times they have consulted that health professional about family history or bowel cancer or screening for bowel cancer. All analyses were conducted in Stata 11.2. Responses to the survey questions were tallied and divided by the total number of participants to calculate proportions, taking the response “Not sure” as a negative response. The characteristics of FDRs associated with having discussed their family history of CRC with a health professional were assessed using logistic regression modelling in a generalized estimation equation framework to account for multiple FDRs per family.

Intensity-modulated radiotherapy (IMRT)

was delivered acc

Intensity-modulated radiotherapy (IMRT)

was delivered according to previously published methods [20]. Hyperfractionated radiotherapy was delivered twice daily at 1.2 Gy per fraction, at least 6 hours apart, 5 days a week. For the purposes of this protocol, IMRT was delivered in two consecutive plans. Over the first 21 treatment days (initial phase), 50.4 Gy was delivered to all targets in 42 twice-daily fractions of 1.2 Gy each. On days 22-32 (radiation boost phase), during which gemcitabine delivery was planned, an additional 26.4 Gy was delivered to the primary tumor and gross nodal CTVs (CTV1s) at 1.2 Gy per fraction, twice daily. The total intended CTV1 dose was 76.8 Gy, delivered over 6.5 weeks Etoposide (64 fractions in 32 treatment days). Doses were prescribed to planning target volumes consisting of 0.5 cm uniform expansions of the CTVs. Target inhomogeneity goals were 99%-107% of the prescribed doses. Gemcitabine was

infused IV over 30 minutes. Five infusions were planned twice weekly during the last 11 treatment days (the radiation boost phase), at least 2 days apart. Toxicity was graded according to the World Health Organization (WHO) scale for hematologic toxicities and the Radiation Therapy Oncology Group (RTOG) scale for nonhematologic toxicities. Grade 3 or 4 toxicities that did not improve to grade 2 or less within 3 months selleck screening library were considered dose-limiting. Late grade 3 esophageal toxicity was considered dose-limiting if it did not improve to grade 2 or less following dilation. In the event of an acute dose-limiting toxicity, or toxicity that required dose-holding, the scheduled gemcitabine treatment was temporarily halted until toxicity declined to grade 2 or less; it was then resumed at the next lower dose

level. Radiation continued without interruption Megestrol Acetate unless there was grade 4 mucositis or skin desquamation that did not respond to supportive measures. In these cases, a break in radiation treatment was allowed. Tumor biopsies to assess the intracellular levels of dFdCTP and dFdCDP, the active metabolites of the drug, were planned 2 hours after the first gemcitabine infusion on day 22. The assessment methods for intracellular phosphorylated metabolites have been detailed previously [8]. Follow-up was conducted 4 weeks after completion of therapy, including clinical assessment for toxicity, history and physical examination, laboratory evaluation of liver and kidney function and complete blood count. Thereafter, patients were evaluated for late toxicity and tumor status every 2 months during the first 2 years and then every 3 to 4 months. At 3 months after completion of treatment, tumor response was assessed by physical examination and CT or PET scans, in addition to direct endoscopy under anesthesia. Complete response was defined as the disappearance of all assessable disease at endoscopy and on images.

An alternative approach to the development of a CMV vaccine has b

An alternative approach to the development of a CMV vaccine has been to utilise DNA vaccination to induce host responses to CMV gB and phosphoprotein 65 (pp65 is another viral target). Recent studies have shown that injection of combinations of plasmids, formulated with an adjuvant, can induce vaccine-specific immune responses, and can

prime for effective memory responses. The hallmark of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) is their ability to establish and maintain latent infection in sensory ganglion neurons. Periodic reactivation of the latent infection results in recurrent infections. Both HSV-1 Ku-0059436 supplier and HSV-2 can cause myriad diseases but the greatest public health problem is genital herpes. Genital HSV-2 infection increases the risk of HIV acquisition and transmission, and control of genital herpes has been predicted to

significantly impact the HIV epidemic. Given the complex natural history of HSV infections, vaccines could have a variety of possible risks and benefits (Table 6.10). An effective HSV SAHA HDAC in vivo vaccine has been sought for more than 80 years. Recently, an HSV-2 glycoprotein D (gD2) candidate vaccine containing the AS04 adjuvant (see Chapter 4 – Vaccine adjuvants), was tested in three large, double-blind, Phase III controlled trials. The first two studies recruited volunteers with a partner with genital herpes disease and found the candidate vaccine was 73% effective against genital herpes disease in women seronegative for both HSV-1 and HSV-2 ( Stanberry et al., 2002). Trends towards protection against infection were also observed, but were not statistically significant. The candidate vaccine was not effective in HSV-1 seropositive women; or in men, regardless of their HSV seropositivity status. These were the first studies to report a significant difference in vaccine efficacy between men and women. This 17-DMAG (Alvespimycin) HCl finding could have important implications for other vaccines targeting sexually transmitted diseases. The basis for this difference could relate to differences in how men and women respond to novel adjuvants or may reflect differences in the acquisition and natural history of

genital herpes in men and women. A third Phase III efficacy trial of the gD2 candidate vaccine in HSV-1 and HSV-2 negative women who thought themselves possibly at risk of acquiring genital herpes (a different risk population than in the original two trials) has been completed and is being analysed. An initial assessment of the results of the third trial showed that the vaccine had an acceptable safety profile but the primary trial endpoint, prevention of genital herpes disease, was not met ( NIAID, 2010). Although the development of the vaccine has been stopped, further analyses and comparison of the trials may guide researchers as they continue seeking vaccines to control HSV infections. As discussed in Chapter 2 – Vaccine immunology, some pathogens have complex life cycles.

For the ROI and PNT averages, we examined the following: (1) conf

For the ROI and PNT averages, we examined the following: (1) confidence intervals around the observed group differences in relation to effects typically observed in similar studies, (2) the power of our study to detect such a typical effect size

and (3) the sample size that would be required to obtain a significant result given our own observed effect size. In each of these calculations, we avoided using both our observed effect size and sample-size-dependent observed statistics at the same time. Details of these power calculations can be found in the Supplementary Methods. Allele frequencies of rs1344706 in these samples were similar to those reported previously (Table 1) [1]. There were no significant deviations from Hardy–Weinberg equilibrium.

No statistically significant differences (all P>.84) between rs1344706 selleck compound genotype groups were found in age, sex, education and IQ for any of the samples, apart from an age difference in the Scottish control sample ( Table 1). In the German sample, voxel-based analysis of FA, MD or regional brain volumetric measures did not result in any significant differences between rs1344706 genotype groups in any brain region either on the voxel level (all PFDR>.37) or on the cluster level (all P>.49; Supplementary Table 1). Similarly, using TBSS, no significant differences in FA were found between the genotype groups in either the control or high-risk samples of the Scottish study

(all P>.38). No significant differences were found in the Scottish control sample after the model was adjusted for the effect of Oxalosuccinic acid age (P>.37). Histograms of raw T-statistics Selleck Panobinostat within the TBSS skeletons were symmetrically distributed around zero. The application of an SVC over the body and genu of corpus callosum did not result in any FA differences between ZNF804A genotype groups using voxel-wise statistics with TFCE (P>.37). Average FA within the corpus callosum ROI also did not differ between genotype groups for the control (T=−0.29, P=.78) and high-risk (T=−0.23, P=.82) groups. Correspondingly, no significant genotype effects were found with PNT for genu in the Scottish samples (controls: T= 0.58, P =.57; high-risk group: T= 0.55, P =.58). Removal of the extreme outlier in the high-risk group did not change this negative result (tractography: T= 0.02, P=.99; ROI: T= 0.20, P=.84). As shown in Fig. 1, there were no trends in either direction for any of the comparisons. Finally, analyses of variance comparing all three genotype groups with respect to average FA within the genu and body of corpus callosum ROI were all nonsignificant, with or without outlier (all F< 0.75, all P>.49), indicating that there were no nonlinear or dominant effects of the risk allele that may have been obscured by combining the CC and AC groups. In summary, whole-brain, TBSS, ROI and PNT results were consistently negative.

The detection of emboli was associated with an increased risk for

The detection of emboli was associated with an increased risk for ipsilateral TIA and stroke (HR 2.54, 95% CI 1.2–5.36) and in particular for ipsilateral stroke (HR 5.57, 95% CI 1.61–19.32) during 2 years of follow-up even after adjusting for antiplatelet therapy, degree of stenosis, and other risk factors. The absolute annual risk of ipsilateral stroke or TIA between baseline and 2 years was 7.13% in patients with embolic signals and 3.04% in those without, and for ipsilateral

stroke was VEGFR inhibitor 3.62% in patients with embolic signals and 0.70% in those without. The authors performed a meta-analysis with all studies available including 1144 patients. The hazard ratio for the risk of ipsilateral stroke for those with embolic signals compared with those without was 6.63 (95% CI 2.85–15.44) with no heterogeneity between studies (p = 0.33). More recently, data from ACES demonstrated that plaque morphology assessed using a simple visual

rating scale predicts ipsilateral stroke in ACS [20]. 435 subjects with ACS ≥70% were included and followed-up for 2 years. A 4-point visual rating scale was applied to the plaques and they were classified as echolucent (37.7%) or echogenic. Plaque echolucency at baseline was associated with an increased risk of ipsilateral stroke alone (HR 6.43, 95% CI 1.36–30.44). A combination of plaque echolucency and ES positivity at baseline was associated with an increased

risk of ipsilateral stroke alone (HR 10.61, 95% CI 2.98–37.82). The combination of ES detection and plaque morphology selleck chemical allows a greater prediction than either measure alone and identifies a high-risk group with an annual stroke risk of 8%, and a low-risk group with a risk of <1% per year. These data SSR128129E show that the combination of 2 measures of plaque instability may identify a high-risk group of patients with ACS that may benefit from a CEA. MRI is a non-invasive method of plaque measurement that does not involve ionizing radiation. Examination of plaque under different contrast weighting (black blood: T1, T2, proton density-weightings, and magnetization prepared rapid gradient echocardiography or bright blood: time of flight) allows characterization of individual plaque components, including lipid-rich necrotic core, fibrous cap status, hemorrhage, and calcification [21]. A few small prospective studies have been done to investigate characteristics of carotid artery plaque on MRI that are associated with disease progression and future cardiovascular events. One study [22] examined patients with symptomatic and asymptomatic carotid disease to determine whether fibrous cap thinning or rupture as identified on MRI were associated with a history of recent transient ischemic attack or stroke.