‘False positive’ catheterization laboratory activations were defined as

those activations that did not meet electrocardiographic criteria for STEMI or those in which no revascularization was required. The definition for DTB time was the time from first registered hospital contact to first intervention that restored blood flow to the culprit vessel. For transferred patients, DTB time was MK-1775 mouse the time from first registered hospital contact at the outside institution as recorded on transfer records. Door-to-call was the time from hospital arrival to the first notification given to the interventional cardiologist on call. Call-to-lab was the time from initial call to arrival at the interventional suite. Call-to-balloon is defined as the time from initial call to the first intervention that restored blood flow to the culprit vessel. Door-to-EKG is the time from hospital arrival to first electrocardiogram

considered to be STEMI qualifying according to preset criteria. EKG-to-call is the time from qualifying electrocardiogram to first call notification of a possible ACS. Other, more detailed parameters recorded in our institution were: Lab-to-balloon, representing time from catheterization suite arrival to first intervention that restored flow to the culprit vessel, lab-to-case start, as time from patient arrival to the interventional suite to time were first invasive action took place (generally initial stick) and case start-to-balloon as the time from first invasive SB203580 purchase action to first intervention that restored blood flow to the culprit vessel. In-hospital major adverse cardiac events (MACE) were defined as the occurrence of death from any cause, Q-wave myocardial infarction Ketanserin (MI) or target lesion revascularization (TLR) before hospital discharge. Q-wave MI is defined as an elevation of creatine kinase-MB ≥3 times the upper normal value in the presence of new pathologic Q waves in ≥2 contiguous leads of the electrocardiogram. TLR

is defined as clinically driven revascularization of the index lesion. PCI angiographic success is defined as a residual stenosis of <30% with thrombolysis in myocardial infarction grade III flow. Clinical success is defined as angiographic success plus the absence of TLR, Q-wave MI, or death prior to hospital discharge. PCI was performed according to guidelines current at the time of the procedure. In all cases, the interventional strategy and the choice of peri-procedural and discharge medications were at the discretion of the responsible physician. Anticoagulation regimens included either bivalirudin 0.75 mg/kg followed by an infusion of 1.75 mg/kg/hour for the duration of the procedure or unfractionated heparin to achieve an activated clotting time of 200–300 seconds in all patients. All patients received an aspirin loading dose of 325 mg and were prescribed 81–325 mg once daily indefinitely.

The patient received a 2-day course of intravenous vancomycin and ceftriaxone, oral prednisolone, and Kefzol eye drops. The hypopyon was completely resolved within 3 days from onset. No Gram staining or cultures were performed, but the mild course and response to steroids suggest that sterile endophthalmitis had occurred. Based on this severe ocular inflammation, the maximum tolerated dose was determined to be 1.0 mg. A second stage of the study that was planned to evaluate repeat doses of MP0112 was not initiated because ocular inflammation was observed and was attributed

Autophagy activator to impurities in the investigative product. AEs noted by the investigator to be related to the procedure were reported in 3 of 32 (9%) patients (conjunctival hemorrhage, vitreous detachment and hypertension, each occurring in 1 patient). Antidrug antibodies were detected in the serum of 8 patients. No further characterization of these was performed. The mean and median CRTs at baseline were 352 μm and 334 μm, respectively (standard deviation, 107.8 μm; range, 191–790) (Table 1). Generally, the higher-dose cohorts experienced a greater decrease in CRT during the 4-week study period (Figure 2). Patients who received 1.0 and 2.0 mg of MP0112 showed the greatest median reductions at week 4 of −95 μm and −111 μm, respectively, compared with

7 μm, −12 μm, and −62 μm in patients who received 0.04 mg, 0.15 mg, and Selleckchem 5FU 0.4 mg, respectively. The overall change in CRT across the dosing cohorts is shown in Figure 2. The initial reduction in CRT observed at week 1 was maintained and further reduced at week 4 in the higher-dose cohorts. Patients receiving 1.0 mg showed median reductions in CRT of −51 μm and −95 μm at weeks 1 and 4, respectively. The median reduction at week 1 in patients receiving 2.0 mg was −6.5 μm. This compared with a median reduction of −111 μm at week 4. In contrast, the CRT of lower-dose cohorts increased or stabilized after an initial decline (Figure 2, center). Patients who received 0.04 mg or 0.15 mg MP0112

had median changes of −33 μm and 7 μm (week 1) or −11 μm and −12 μm (week 4), respectively. The VA remained stable (defined as loss of <15 letters compared with baseline) 17-DMAG (Alvespimycin) HCl and did not vary from baseline in all dosing cohorts across the study period. Up to 100% of patients experienced either no loss in VA or a gain from baseline in letters on the ETDRS charts at each time point (94%, 97%, 94%, 91%, 91%, and 100% of patients at weeks 1, 2, 4, 8, 12, and 16, respectively). Of 32 patients, 4 (12.5%) experienced reversible loss of ≥15 letters secondary to inflammation at various time points. At initial screening, FA showed that patients had both mean and median leakage areas of 11.5 mm2 (±5.1; range, 1.6–20.8) across dose cohorts. At week 4, the mean and median leakage areas had decreased to 2.4 mm2 and 0 mm2, respectively (±3.8; range, 0–14.3) (Figure 3). FA also demonstrated a mean decrease in lesion size from 11.1 mm2 (median, 10.

68–1.39 (br m, 4H, DAPT manufacturer 2× –CH2), 1.17 (d, 6H, J = 6.1 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.04 (s, 6H, 2× –CH3); 13C NMR (CDCl3, 75 MHz): δ 167.2, 158.6, 144.6, 128.1, 123.2, 116.8, 113.3, 79.8,

72.2, 66.6, 53.1, 51.6, 35.8, 30.3, 25.6, 23.3, 18.4, −4.7; IR (neat): 2938, 1729, 1608, 1512, 1451, 1379, 1164, 1038 cm−1. To a solution of 17 (3.0 g, 7.08 mmol) in THF:MeOH:water (3:1:1, 20 mL), LiOH (0.51 g, 21.25 mmol) was added and stirred at room temperature for 4 h. The pH of reaction mixture was adjusted to acidic with 1N HCl solution and extracted with ethyl acetate (40 mL). Organic layers were washed with water (15 mL), brine (15 mL), dried (Na2SO4), evaporated under reduced pressure to give 18 (2.28 g, 79%) as a colorless oil, [α]D −12.1 (c 1.2, CHCl3); 1H NMR (CDCl3, 300 MHz): δ 7.20 (d, 2H, J = 8.0 Hz, ArH-PMB), 6.89 (dd, 1H, J = 6.2, 15.7 Hz, olefinic), 6.84 (d, 2H, J = 8.0 Hz, ArH-PMB), 5.71 (d, this website 1H, J = 15.7 Hz, olefinic),

4.31 (d, 1H, J = 11.5 Hz, benzylic), 4.16 (d, 1H, J = 11.5 Hz, benzylic), 3.83 (m, 1H, –OCH), 3.67 (s, 3H, OCH3), 3.47 (m, 1H, –OCH), 1.67–1.52 (m, 2H, –CH2), 1.49 (m, 2H, –CH2), 1.07 (d, 6H, J = 6.1 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.06 (s, 6H, 2× –CH3); 13C NMR (75 MHz, CDCl3): δ 170.1, 158.4, 149.1, 130.1, 128.0, 117.6, 113.8, 76.1, 73.2, 66.2, 55.7, 38.2, 30.3, 26.3, 24.2, 17.5, −4.3; IR (neat): 3449, 3031, 2930, 2857, 1710, 1097 cm−1. To a cooled (0 °C) solution of 18 (1.75 g, 4.27 mmol) in dry THF (15 mL) under nitrogen atmosphere, TBAF (5.13 mL, 5.17 mmol) was added and stirred for 3 h. After completion of reaction, reaction mixture was diluted with water (5 mL) and extracted with ethyl acetate (2 × 40 mL). Organic layers were washed with water (2 × 10 mL), isothipendyl brine (10 mL), dried (Na2SO4), evaporated to give 8 (1.08 g, 86%)

as a liquid. [α]D +35.4 (c 1.0, CHCl3); δ 7.17 (d, 2H, J = 8.2 Hz, ArH-PMB), 6.88 (dd, 1H, J = 6.1, 15.8 Hz, olefinic), 6.84 (d, 2H, J = 8.2 Hz, ArH-PMB), 5.70 (d, 1H, J = 15.8 Hz, olefinic), 4.31 (d, 1H, J = 11.5 Hz, benzylic), 4.16 (d, 1H, J = 11.5 Hz, benzylic), 4.07–3.89 (m, 1H, –OCH), 3.82 (m, 1H, –OCH), 3.66 (s, 3H, OCH3), 1.67–1.49 (m, 2H, –CH2), 1.47–1.36 (m, 2H, –CH2), 1.07 (d, 6H, J = 6.0 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.01 (s, 6H, 2× –CH3); 13C NMR (CDCl3, 150 MHz): δ 172.3, 158.1, 146.4, 132.6, 128.1, 119.1, 112.8, 78.9, 70.3, 68.6, 56.2, 34.9, 29.8, 23.6; IR (neat): 3451, 2929, 2857, 2102, 1722, 1612, 1514, 1360, 1041, 777 cm−1.

Their model may therefore underestimate the number of symptomatic infections observed. Secondly, the models differ in assumptions regarding immunity and re-infection. The model Osimertinib mouse presented here assumes that a fraction of individuals gain long-term immunity after each episode of disease. Pitzer et al. assumed a period of temporary but complete immunity after each infection waning at a constant rate with a mean duration of 9–12 months. We chose not to assume a period of complete protection, as studies looking at protection

conferred by natural infection in children have shown that up to four re-infections are possible within a two-year study period [15] and [18]. Thirdly, supported by household studies [19], [20], [21] and [22], we assumed that only symptomatic individuals are infectious and important in transmission, whereas Pitzer et al. assumed that all infections, to varying degrees, play a role in transmission (symptomatic infections > asymptomatic infections). In addition, we modelled all symptomatic infections in the population as opposed to modelling only severe symptomatic infections and, unlike Pitzer et al., we had an independent estimate of the reporting efficiency (under-ascertainment of rotavirus disease cases within the surveillance data), and so we did not have to estimate this and the transmission parameters (which could pose identifiability problems). In addition, we used a detailed dataset

learn more on contact patterns for Great Britain to improve parameterisation of the model and to help inform assumptions about mixing patterns between age groups. Despite these differences in model assumptions, the results of our model regarding the effect of vaccination are very similar to those of Pitzer et al., suggesting that the results are robust to slight differences in model structure.

Pitzer et al. also demonstrated that spatiotemporal variations in the size and timing of the peak in rotavirus disease could be explained by variations in birth rate. We incorporated into our model year-specific birth rates for England and Wales between 1998 and 2007. It did not improve the fit of the model or predict the slight fluctuations in the size or timing of the epidemics seen from year to year. Variability in birth rates over time observed in England and Wales are less marked than those in the United Metalloexopeptidase States. This could explain why, unlike in the model developed by Pitzer et al., varying annual birth rates in our model was not important. Our model predicts that there will be an increasing decline in numbers of reported cases and delay in the start of the season in the first two years post-vaccination. Interestingly, a slight increase in numbers is predicted in the third post-vaccination year compared to the second. These predicted early dynamics capture the observed effects of vaccination seen in the United States [36] and [37] and are similar to those predicted by Pitzer et al. [29].

The reaction was detected with a secondary antibody HRP conjugated anti-human IgG (Chemicon, Australia) and enzyme substrate solution, TMB (3,3′,5,5′-tetramethylbenzidine, KPL, USA) followed by a 1 M H3PO4 stop solution. The absorbance (OD) was measured at 450 nm (reference filter 630 nm) on a Bio-Tek Elx808 (Bio-Tek Instruments, USA). OD was converted to antibody concentrations (μg/ml) using KCJunior software (Bio-Tek Instruments, USA). Sample dilutions were analyzed in duplicate and three controls (low, medium and high) were included on each plate to assess assay performance and inter-assay

variation. Results from HDAC inhibitor an inter-laboratory comparison between Wyeth Vaccines and the KTL Finland laboratory demonstrated a good correlation in measurement of serotype-specific antibody concentrations [28]. Laboratory staff members were

blinded to the group allocation of each serum sample. Cleaned data were exported to Stata version 9.0 (Stata Corporation, College Station, Texas) for analysis. Serotype-specific Protein Tyrosine Kinase inhibitor antibody concentrations by ELISA were log transformed (to base e) to calculate GMC. Comparisons of pre- and post-mPPS GMC and between group comparisons were performed using a paired t-test and two sample t-test, respectively. Simple and multi-variable regression analyses were undertaken to adjust for both the pre-mPPS log antibody concentration for all 23 serotypes, and the number of PCV doses check administered for all seven PCV serotypes. A p-value of <0.05 was considered statistically significant. The primary endpoint was serotype-specific

GMC response to mPPS at 18 months of age in children who had received the 12 months 23vPPS compared to children who had not received the 23vPPS. We defined hyporesponsiveness to a particular serotype as a significantly lower GMC observed post-mPPS, in the 12 month 23vPPS group compared to the no 12 month 23vPPS group, controlling for pre-mPPS antibody levels, using multivariable regression analysis. To prevent an inflated type 1 error due to multiple comparisons, and obtain a single p-value for the null hypothesis of mPPS having no impact on the antibody response to any of the 23 serotypes, a joint test of all the regression coefficients from the aforementioned multivariable regression analysis was performed [29]. The study was approved by the Fiji National Research Ethics Review Committee and the University of Melbourne Human Research Ethics Committee. There were 552 children enrolled in the study (Fig. 1) which represent a consent rate of 30.5%. There were 90 (16.3%) withdrawals and no child was withdrawn due to an adverse event resulting from administration of any of the vaccines. Characteristics and the number of children randomized to the eight groups are shown in Table 1. Following the 12 month 23vPPS, there were significantly higher GMC (each p < 0.001) for all PCV serotypes.

The network now includes 30 clinical recruitment sites or hospitals, eight regional laboratories and four referral laboratories located in different parts of India, including high-mortality burden states such as Bihar and Odisha (Fig. 2). The goal of the network is not only to collect more data but also to establish a model surveillance system for a vaccine preventable disease based on which further studies to evaluate the impact of vaccination can be conducted. There are several steps being undertaken to enhance the quality of the surveillance system and these include i) providing training

to clinical and laboratory staff and written guidance using jointly developed standard operating procedures, Going forward, the use of the rotavirus surveillance

network established by ICMR will need to reflect the priorities of DAPT cell line the government of India. The network has already yielded results in estimating the burden of disease and its seasonal variation. The network is also a readily available platform to inform decision-makers for vaccine introduction into the immunization programme and for further studies to monitor the this website impact of vaccine. While broad heterotypic protection from rotavirus vaccination is expected based on pre- and post-licensure data from other settings, effectiveness assessments and rotavirus strain monitoring after vaccine introduction will continue to be important. None. “
“Vaccines are widely recognized as one of medicine’s greatest achievements. Without vaccinations, millions of children and adults would contract a range of serious diseases that are now prevented by vaccines, and many would have long-lasting

effects, like the polio affected children most older Indians grew up with, or even die. Vaccination is one of the most important tools in public health, protecting individuals and communities from disease, and the range 17-DMAG (Alvespimycin) HCl of diseases that can be prevented by vaccines is expanding across and beyond infectious diseases. Research has shown there are powerful links between population health and economic well-being. Childhood vaccination in particular is a valuable investment because it not only reduces morbidity and mortality in a country but also promotes national economic growth and poverty reduction [1]. Until a few decades ago, new vaccines were developed and made in the first world, by large companies, who focused on the markets from which they could derive maximal return on investment. This led to a situation where the bulk of disease lay in poorer countries while the vaccine supply, limited in amount and by price, was mainly in countries with low disease burden and high purchasing power.

Other vaccine attempts NVP-BKM120 cell line have included a variety of subunit vaccines, none of which provided complete protection against heterologous challenge [3] and [4]. In addition, while infection with one strain of A. marginale sensu stricto typically precludes infection with another, multiple cases of superinfection have been described [5], [6] and [7]. Vaccine failures are due to expression of variants of the major surface proteins

MSP2 and MSP3. A. marginale creates a wide array of antigenic variants by substitution of whole or partial pseudogene cassettes into a single genomic expression site by segmental gene conversion [8], [9], [10] and [11], with increasing complexity of the expressed mosaic proteins [12]. Following persistent infection, the immune system has

Ku-0059436 order been exposed to a majority of the simple variants, which prevents another strain with similar variants from establishing concurrent infection. However, if the second strain has a unique pseudogene, novel variants generated by segmental gene conversion allow superinfection to take place [13]. In addition to MSP2 and MSP3, a variety of other variable surface antigens have been found in A. marginale; these have been called the msp2 superfamily [14]. Generally, these are all members of the pfam01617 (Surface Ag 2), which has related members in several other bacterial genera. Several of these have been found in cross-linked surface antigen complexes, and have been suggested as vaccine candidates [15]. A recent study by Agnes et al. used sera from cattle infected with A. marginale subspecies centrale to determine antigens that are cross-protective from sensu stricto challenge [16]. Several other studies have implicated components of the bacterial type 4 secretion system as vaccine candidates [17], [18] and [19]. In this paper, we examine multiple strains of A. marginale sensu

stricto, using high-throughput sequencing techniques to examine the members of unless the pfam01617 family and the other previously suggested vaccine components to determine their degree of conservation. Proteins that are widely conserved between all strains are candidates for inclusion in cross-protective vaccines. Further, the techniques described can be used to examine other organisms with significant numbers of repeats, allowing rapid determination of conserved proteins for diagnosis and vaccine development. A. marginale genomic DNA was isolated from highly infected bovine blood taken at the acute stage of infection. Organisms were purified from uninfected erythrocytes and white cells by passage through a cellulose column (C-6288, Sigma, St. Louis, MO) and frozen [20]. Genomic DNA was isolated from organisms using Qiagen genomic DNA kits according to manufacturer protocols.

As depicted in Fig. 1, the 2007 outbreak strains formed a distinct cluster within G9 VP7 Lineage III, sub-lineage D. The strains in Lineage III exhibited 93.3-99.1% nucleotide identity

to the Alice Springs outbreak samples. The 2007 outbreak strains exhibited closest similarity to a G9P[8] strain isolated in Brazil in 2006, with 99.0–99.1% nucleotide similarity and 99.8–99.9% amino acid identity. PD0332991 Comparison of the deduced amino acid sequences of the VP7 genes from the 2007 outbreak strains with VP7 from G9P[8] strains previously identified in Australia also revealed a close relationship with the previous circulating Australian G9P[8] strains in Lineage III, with a 98.0–98.7% nucleotide and 94.0–96.3% amino acid sequence similarity observed. Three conserved amino acid substitutions were identified at positions 44 (Ala/Val-Thr), 263 (Val-Ile) and 279 (Ala-Thr) in the GSK1210151A solubility dmso 2007 outbreak strains when compared to other G9 strains analysed. A 663 bp region of the VP8* subunit of the VP4 gene was sequenced for six G9P[8] samples, including three from vaccinated infants.

The sequences were highly conserved with 99.6–100% nucleotide identity and 98.7% amino acid homology observed. No conserved nucleotide or amino acid changes were observed between samples obtained from vaccinated and non-vaccinated patients. Phylogenetic analysis of the nucleotide sequence of the VP8* subunit of the G9P[8] 2007 outbreak strains and previously published P[8] human strains was performed. As depicted in Fig. 2, through the 2007 outbreak strains formed a distinct cluster within P[8] Lineage 3 (P[8]-3). The strains in P[8] Lineage 3 exhibited 97.3–99.7%

nucleotide identity to the Alice Springs outbreak samples. The 2007 outbreak strains revealed close similarity to G9P[8] strains isolated in the USA, Russia and Ireland, displaying 98.6–99.3% nucleotide and 97.0–99.1% amino acid identity. When compared to a 2001 Australian G9P[8] isolate, the outbreak strains exhibited 98.3–98.6% nucleotide and 97.8–98.7% amino acid identity. The 2007 outbreak strains contained two unique amino acid substitutions at positions 237 (Ser-Leu) and 242 (Thr-Ser) when compared to all other P[8] strains analysed. The 750 bp of the NSP4 gene was sequenced for 14 G9P[8] outbreak strains including three from vaccinated infants. The sequences were all highly conserved displaying 99.4–100% nucleotide and 99.9–100% amino acid identity. No conserved changes were observed between samples obtained from vaccinated and non-vaccinated patients. Phylogenetic analysis of the nucleotide sequence of the NSP4 gene of the G9P[8] 2007 outbreak strains and previously published NSP4 genes was performed. As depicted in Fig. 3, the NSP4 from the 2007 outbreak strains formed a distinct cluster within the E1 Genogroup. The strains in E1 Genogroup exhibited 90.6–99.

MPI Research is accredited by the Association for Assessment and Accreditation of Laboratory ATM inhibitor cancer Animal Care International (AAALAC International), and was under guidance of IACUC. Vaccinations with the nanoparticle vaccine and saline control were administered by injection between the skin and underlying layers of tissue in the thigh region of each animal. The same injection site on each animal was used for each administration unless a reaction at the injection site indicated that another site must be used. All injection sites were marked and identified throughout the course of

the study. The dose was administered by bolus injection. Monkeys were immunized (N = 10 per group) on days −78 and −48 with a combined pediatric diphtheria/tetanus

toxoid vaccine, and then immunized on days 1, 29, and 57 with saline, or escalating doses of 1 mL of nanoparticle vaccine at 0.5, 2.0, 8.0 and 16.0 mg/mL. Blood was collected on days shown, prior to immunization (day 1) and then on days 29, 57, 85, 113, and 141 to test for anti-nicotine antibodies. Peripheral blood was collected on day 85 for T cell recall analysis (3 mL) and PBMC isolated by percoll centrifugation. Briefly, human peripheral blood mononuclear cells (PBMCs) were isolated from normal human donors (Research Blood Components, Cambridge, MA). Blood was check details diluted 1:1 in phosphate buffered saline and then 35 mL overlaid on top of 12 mLs Ficoll-Paque premium

(GE Healthcare, Pittsburgh, PA) in a 50 mL centrifuge tube. Tubes were spun at 1400 RPM for 30 min, and the transition phase PBMCs collected, diluted in PBS with 2% fetal calf serum and spun at 1200 rpm for 10 min. Cells were re-suspended in cell freezing media (Sigma–Aldrich, St. Louis, MO) and immediately frozen at −80 °C. For long term storage, cells were transferred to liquid nitrogen. For rhesus monkey PBMC isolation the protocol was the same except 5 mL of blood was collected and processed. Idoxuridine For cynomolgus monkey PBMC, 3 mL of blood was processed, buffy coat was collected and overlaid on 60% Percoll (GE Healthcare), centrifuged 30 min at 1755 rpm, washed and frozen as described above. Frozen PBMC were thawed (37 °C water bath), re-suspended in PBS 10% FCS, spun down and re-suspended to 5 × 106 cells/mL in tissue culture media (RPMI), supplemented with 5% heat inactivated human serum (Sigma–Aldrich), l-glutamine, penicillin and streptomycin, (Gibco, Grand Island, NY). For memory T cell recall response assays, cells (0.6–1.0 mL) were cultured in 24-well plates with 4 μM peptide (GenScript) at 37 °C 5% CO2 for 2 h. One μL of 1000× Brefeldin A (BD, San Jose, CA) per mL of culture media was then added and cells returned to a 37 °C incubator for 4–6 h. Cells were then incubated at 27 °C, 5% CO2 for 16 h.

200-2007-22643-003). CDC staff has reviewed the project’s evaluation design and data collection methodology and the article for scientific accuracy. All authors have read and approved the final version. “
“To stem and reverse childhood obesity, a number of policymakers and public health authorities at the federal, state,

and local levels have intensified their efforts to improve the nutritional quality of school meals through the establishment of institutional policies or practices that promote healthy food procurement (Institute of Medicine, 2010 and United States Department of Agriculture, 2012). These practices have included such strategies as setting upper limits for calories, sodium, and other nutrients per serving in the contracts of

food services vendors; institutional find more procurement of healthier options such as whole grains and plant-based foods; and/or complementary approaches such as nutrition education, signage, and product placement to increase student selection of healthy food. Collectively, these institutional practices aim to improve the quality of foods served in schools, increase food security, and positively influence student dietary intake (IOM, 2010). The Los Angeles Unified School District (LAUSD), the second largest school district in the United States, serves more than 650,000 meals per day. With such volume and purchasing power, LAUSD has become a national leader in increasing student access to

healthy foods through changes to its school meal program (Cummings et al., 2014). Tofacitinib mouse In the 2011–2012 school year (SY), the LAUSD Food Services Branch (FSB) launched a new menu that included more fresh fruits and vegetables, whole grains, vegetarian items, and a range of ethnic foods; it also eliminated flavored milk. These menu changes currently exceed the USDA school Final Rule on school meal nutrition standards, released in 2012 (USDA, 2012). In developing the revised menu, LAUSD held community taste tests during the summer of 2011 at its central kitchen. While taste testing TCL results suggest that students reacted favorably to the new menu options, there were anecdotal reports that students reacted negatively when the meals were served in the actual school cafeterias (Wantanabe, 2011). The national Communities Putting Prevention to Work (CPPW) program, funded by the Centers for Disease Control and Prevention (CDC), supports increasing access to healthier food options, including establishing healthy food procurement practices in schools ( Bunnell et al., 2012). Despite growing support for such school-based practices ( Institute of Medicine, 2010 and Story et al., 2008), limited evidence exists to support the effectiveness of such efforts for changing student food selection and eating behaviors. A key question is how students react to these changes to the menu.