The present sub-study aimed at investigating the immunological effects of OPV together with BCG at birth on the developing immune response at 2, 4 and 6 weeks of age, including innate and non-polio specific adaptive responses, non-specific inflammation markers and immune

cell distribution. Our a priori hypothesis was that OPV would dampen the IFN-γ response to PPD. The present immunological study was carried out within a larger RCT investigating Galunisertib cost the effects of providing OPV0 with BCG at birth on infant survival. The trial was conducted from July 2008 to October 2011 at the Bandim Health Project (BHP), a health and demographic surveillance system site covering six suburban districts of Bissau, the capital of Guinea-Bissau, West Africa. The trial has been described elsewhere (Lund, submitted; clinicaltrials.gov: NCT00710983). Everolimus concentration In brief, newborns with no overt illness or malformations, weighing ≥ 2.5 kg at enrolment and living in the BHP study area were eligible for recruitment. Mothers received oral and written information. Provided consent, the mother drew a randomisation number allocating her infant

to receive OPV0 together with the BCG (OPV0 + BCG) or BCG alone (BCG). The BCG (Danish strain 1331, Statens Serum Institut, Copenhagen, Denmark) was given intra-dermally in the upper left deltoid region while the trivalent OPV was administered as two drops orally. below From 27 May 2009 to 7 April 2010, infants delivered on weekdays at the maternity ward at the Simão Mendes National Hospital and randomised within the first 7 days of life were invited to participate in the present immunological sub-study, excluding infants delivered by caesarean section or twins. During the synchronised West African Polio Immunisation Campaigns in March and April 2010 some infants were not included (n = 32) ( Fig. 1). Informed consent was obtained according to the same procedure as the main trial. Measurements of weight, length,

circumferences of abdomen, head and mid-upper-arm and axillary temperature of the infant, and axillary temperature of the mother were obtained at enrolment. Subsequently, the infants were randomised to a follow-up visit at home at 2, 4 or 6 weeks after enrolment. Infants who received other vaccines before blood sampling were excluded from the study (Fig. 1). At the follow-up visit at 2, 4 or 6 weeks a blood sample was collected, the mother was interviewed about the health of her infant; the mid-upper-arm circumference and axillary temperature of the infant were measured; formation of scar or local reaction at the site of BCG vaccination was recorded (yes or no). Additionally, the main trial also recorded the presence and size of BCG scar at 2, 6 and 12 months after enrolment on the same infants.

“
“Cancer is the abnormal disease, which affect the normal cell growth inside the body. The cascade expression of multiple Gefitinib datasheet genes and protein paves complications to cure the disease. There are few important crucial proteins are primary source for either inducing or suppressing the gene and protein expression. Currently kinases based proteins are taken as drug targets for treating the cancer because kinase signaling from one receptor to another receptor in cancer cell is more rapid and it leads to tremendous growth of the cancer cells in the body. The screening of lead compounds in invitro and invivo studies takes more time and cost for screening the compounds. Drug discovery

through computational tools and software’s reduces the time span of the drug candidate in the pharmacy market. One of the approaches

to analog-based drug discovery is the concept of ‘Bioisosteric Replacement’ in the design of novel pharmacological tools as well as new therapeutic agents with optimal pharmacological profile and improved pharmacokinetic properties.1 Benzothiazepines are seven member heterocyclic compounds that are bioisosters of benzodiazepines and contain one sulfur in place of nitrogen have received consideration in recent years. It is only that recent attention is being directed to a variety of synthetic methods due to its selleck kinase inhibitor efficient therapeutic properties. Benzothiazepines posses wide variety of activities like anticonvulsant2 CNS depressant,3 and 4 isothipendyl Ca++ channel blockers,5 anticancer,6 anti fungal,7 anti-HIV8 and antimicrobial9 etc. Dong et al reported that the discovery of tetra cyclic benzothiazepines (BTZs) as highly potent and selective antimalarial along with the identification of the Plasmodium falciparum cytochrome b, c (1) complex as the primary functional target this class of compounds.10 The Benzothiazepine function is quite stable and has inspired chemists to utilize this stable fragment in bioactive

moieties to synthesize new compounds possessing biological activities. All compounds synthesized by coupling of substituted 2-aminothiophenol and α-oxoketene dithioacetals. In this current study, the benzothiazepines and its analogs were taken and targeted for the mitogen activated protein kinase using Insilco molecular docking tools. All commercially available reagents were obtained from various producers and used without further purification. Reaction was monitoring using TLC (silica gel 60 F254, Merck) plates. Microwave irradiation done in Biotage (Initiator Eight, 900 W at 2450 MHz). The NMR spectra were recorded with a Bruker AC (300 MHz) spectrometer, with TMS as internal standard, the chemical shift (δ) and coupling constant (J) values were expressed in ppm and Hz only. The mass spectra (EI) were recorded at 70 eV with a Shimadzu ESI-Mass spectrometer. Unless otherwise mentioned, the organic extracts were dried over anhydrous Na2SO4.

17 Ahmad et al reported that synthesis of triheterocyclic 4H-pyrimido[2,1-b]benzothiazole ring systems by using one pot three component

Imatinib purchase reaction. Reactions were monitored by thin layer chromatography using silica gel-G as adsorbent using benzene as mobile phase. IR spectra (KBr pellet) were recorded on Bruker α FT-IR spectrometer, at Amrutvahini College of Pharmacy, Sangamner. 1H NMR spectra (DMSO-d6) were taken on NMR Bruker (Swiss) Avance II 400 MHz spectrometer from Punjab University,

Chandigarh. Equimolar mixture of ethyl cynoacetate, (0.01 mol) substituted benzaldehyde (0.01 mol); substituted 2-amino benzothiazole (0.01 mol) and 25 ml ethanol in RBF were SCR7 irradiated independently inside microwave oven at 640 W for 5 min (TLC control). The crystalline product was started to separate out just after cooling the reaction mixture at room temperature. The crystalline solid that separated out was filtered and found to be pure by TLC. Recrystallization was done with ethanol. Physicochemical properties of all synthesized compounds depicted in Table 1. FT-IR (KBr): 3425(N–H str), 3036(C–H str), 1723(C O str), 1610(C N str), 1534(C C str),1266(C–S

str), 727(C–Cl str).1H NMR (DMSO-d6) δ ppm:, 1.34–1.38(t,3H,CH3), δ3.35(s,2H,NH2), δ4.29–4.35(q,2H,CH2), δ6.12(s,1H,CH), δ7.71–7.93(m,3H,Ar H), δ7.48(m,4H,Ar H)., EI–MS: (m/z:, %RA): 419(M+ 92%),418(M+2 56%); % Anal.: calculated: crotamiton C 54.29,H 3.60%,N 10.00%,O 7.61% Found: C 54.32%,H 3.46%,N 9.06%,O 7.52%. FT-IR (KBr): 3418(N–H str), 3030(C–H str), 1719(C O str), 1606(C N str), 1540(C C str), 1528(–NO2str), 1267(C–S str). 1H NMR (DMSO-d6) δ ppm:, δ 1.33–1.37(t,3H,CH3), δ 4.12(s,2H,NH2), δ4.32(q,2H,CH2), δ 6.16(s,1H,CH), δ 7.61–7.73(m,4H,Ar H), δ 7.94(m,3H,Ar H)., EI–MS: (m/z:RA): 429(M+ 87%),427(M+2 48%); % Anal.: calculated for C 52.96%,H 3.51%,N 13.00%,O 14.85%,Found: C 52.78%,H 3.72%, N 13.06%,O 14.56%. FT–IR (KBr): 3455(N–H str), 3324(–OH str), 3021(C–H str), 1714(C O str), 1645(C N str), 1540(C C str),1270(C–S str). 1H NMR (DMSO-d6) δ ppm:, δ 1.31–1.36 δ(t,3H,CH3), δ 3.35(s,2H,NH2), δ 4.27–4.32(q,2H,CH2), δ 6.21(s,1H,CH), δ 5.1(s,1H,OH), δ 7.70–7.85(m,3H,Ar H), δ 7.90(m,4H,Ar H). EI–MS: (m/z: RA): 400(M+ 71%), 398(M+2 52%); % Anal.: calculated: C 56.79%,H 4.01%, N 10.46%,O 11.94%, Found: C 56.82%,H 4.00%.N 10.36%,O 11.78%. FT–IR (KBr): 3455(N–H str), 3284(–OH str), 2987(C–H str), 1723(C O str), 1585(C N str), 1270(C–S str).

57 ± 6.1 mg/dL) with approx. 47% decrease, HDL (11.86 ± 2.4) with 45% selleck compound increase and LDL (16.07 ± 8.6 mg/dL) with approx. 70% decrease over acetaminophen treated group and being comparable with the group treated with silymarin. Tinospora sinensis had specific effect on improvements in SGPT (176.60 ± 4.4 U/mL), ALP (22.13 ± 6.5 U/mL) with 58% decrease, VLDL (16.43 ± 2.6 mg/dL) and Triglyceride levels (82.15 ± 13 mg/dL) with 40% decrease when compared with acetaminophen treated group. It may be noted that the levels of VLDL and triglycerides in Tinospora sinensis treated group are found to be statistically insignificant when compared to silymarin treated

group, and hence are comparable to positive control. Neem guduchi was found to have specific effect on SGOT (147.43 ± 18.9) and bilirubin (1.05 ± 0.1) levels. The differential hepatoprotective effects of guduchi satwa prepared from these three Tinospora species are also evident from liver histology ( Fig. 1 a–f). The liver histology of the animals treated with T. cordifolia satwa exhibit improvements over acetaminophen treated group ( Fig. 1d) but with intermittently swollen centrilobular hepatocytes which are more prone to ischemic injury while periportal hepatocytes appear normal. The liver histology of the group treated with T. sinensis www.selleckchem.com/products/KU-55933.html exhibits near normal histology ( Fig. 1e) with prominent

hepato-regeneration as evident from distribution of normal hepatocytes among degenerating swollen hepatocytes. This group also shows normal periportal hepatocytes. The liver histology of Neem guduchi satwa treated group ( Fig. 1f) is strikingly normal without any histologically detectable anomalies. The liver disorders are treated with an aim to prevent degeneration of hepatocytes and consequent metabolic derailments and to promote regeneration

of hepatocytes.3 Overdose of acetaminophen is known to have hepatotoxic effects which is reflected at the biochemical as well as histological level in the form of altered liver function tests and mild to severe alterations in the histological architecture first of hepatocytes. Tinospora is known to exhibit potent hepatoprotective and immunomodulatory activities. 19, 20, 21 and 22 The majority of studies on hepatic injury are found to be based on acute dosing of hepatotoxicant 23, 24, 25 and 26 and indicating the effect of Tinospora or other phytomedicines in alleviating hepatic injury. It is also known that the repeated dosing of acetaminophen, even for four days in male Sprague–Dawley rats leads to development of physiological adaptation to overdose of acetaminophen. 27 Hence care must be taken to design the animal experiments when considering acetaminophen as heptotoxicant, in order to avoid the dosage levels leading to development of physiological adaptation which may be mistaken as a hepatoprotective effect of the agent under investigation.

gondii. In the present work, we constructed recombinant Influenza A viruses harboring a dicistronic neuraminidase segment encoding T. gondii tachizoyte surface antigen SAG2 under control of a duplicated internally located 3′ promoter. Recombinant FLU-SAG2 viruses were genetically stable and induced expression of SAG2 in cell culture as well as in lungs of infected mice. We also observed that FLU-SAG2 was immunogenic

and, when associated with recombinant adenoviruses expressing SAG2 in vaccination protocols, elicited humoral and cellular anti-SAG2 immune responses, conferring a high degree of protection against challenge infection screening assay with the P-Br strain of T. gondii. Previous studies demonstrated that sequence of vector administration has pivotal importance in induction of heterospecific immune response in heterologous vaccination protocols [13], [14], [47] and [50]. Indeed, Li and co-workers showed that mice primed with a recombinant influenza and boosted with recombinant

Vaccinia encoding CS antigen, were protected after challenge with Plasmodium. However, no protection was observed in mice primed with Vaccinia and boosted with influenza. According to the authors, the systemic boost with Vaccinia could induce CTL migration to the liver, where Plasmodium circumsporozoyte replication occurs, while the intranasal boost with influenza viruses Selleck PLX3397 would favor CTL migration to lungs [13]. Based on these previous observations, we have chosen to prime the animals with FLU-SAG2 and to boost with Ad-SAG2. We speculate that the influenza vector would elicit anti-SAG2 immune response mainly at the respiratory level, priming both B and T cells, whereas a boost with adenovirus would reinforce the response at systemic level. Indeed, detection of IFN-γ producing

T cells specific for SAG2 in spleen and protection after challenge infection were only demonstrated in mice that received Ad-SAG2 boost by subcutaneous route. Although we did not evaluate the cellular immune response in respiratory tract, we speculate that boosting by intranasal route could detour T lymphocytes to respiratory tract and to abrogate the systemic cellular immune response. In our experiments, mice primed through with FLU-SAG2 and boosted with recombinant Ad-SAG2 displayed significant reduction of parasite burden after challenge with the P-Br strain of T. gondii. On the other hand, mice vaccinated with a single dose of Ad-SAG2 showed parasite burden similar to that found in animals vaccinated with control vectors. These results support previous studies showing that often significant protection cannot be achieved after a single immunization [3] and [51]. In addition, our results showed that innate immune response triggered by influenza inoculation was not sufficient to explain protection observed after the boost with Ad-SAG2.

31

Another portion of wet liver tissue was used for the estimation of glycogen content.32 The TCA cycle enzymes were also assayed. Isocitrate dehydrogenase enzyme activity was assayed according to the method of Bell and Baron.33 α-Ketoglutarate dehydrogenase enzyme activity was estimated selleck according to the method of Reed and Mukherjee.34 Succinate dehydrogenase enzyme activity was estimated according to the method of Slater and Bonner.35 Malate dehydrogenase activity of malate dehydrogenase was assayed by the method of Mehler et al.36 The results were expressed as mean ± S.E.M of six rats per group and statistical significance was evaluated by one way analysis of variance (ANOVA) using SPSS (version 16.0) program followed by LSD. Table 1 shows the qualitative analysis of phytochemicals present in the ethanolic extract of Mengkudu fruits. From preliminary secondary metabolites screening, it was found that the extract showed a positive response for the presence of flavonoids, alkaloids, glycosides, saponins, proteins, triterpenoids and phenols. Table 2 and Fig. 1 portray the effect of oral administration of MFE on blood glucose, Hemoglobin, glycosylated hemoglobin, plasma insulin, and C-peptide levels in experimental groups

of animals. There was a significant elevation in the levels of blood glucose and glycosylated hemoglobin and concomitant fall in Hb of STZ induced diabetic rats as compared Selinexor supplier with control group of rats. Upon treatment with MFE as well as gliclazide for 30 days, diabetic rats showed a significant decrease in the levels of blood glucose and glycosylated hemoglobin, and proportionate rise in Hb, which were comparable with control group of rats. Moreover, the significantly diminished plasma very insulin and C-peptide levels of diabetic rats were improved substantially to near normal level by the administration with MFE as well as gliclazide. Tables 3 and 4 depict the outcome of

MFE supplementation on the activities of hexokinase, pyruvate kinase, LDH, glucose-6-phosphatase, fructose-1, 6-bisphosphatase and glucose-6-phosphate dehydrogenase in liver and kidney tissues of control and experimental groups of rats. The enzymes activities were altered in liver and kidney tissues of STZ induced diabetic rats. Upon treatment with MFE as well as gliclazide for 30 days, diabetic rats improved from the altered enzyme activities to near normalcy in liver and kidney tissues. Tables 5 and 6 represents the activities of TCA cycle key enzymes in liver and kidney tissues of control and experimental groups of rats. The liver and kidney tissues of diabetic rats showed momentous depleted activities of isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase.

After removing the medium, find protocol splenocytes from individual mice at a density of 105 cells/well were stimulated with a pool of CSp peptides at a concentration of 5 μg/well for 48 h at 37 °C 5% CO2. Following incubation, plates were washed five times with PBS and were then incubated with 1 μg/ml of biotinylated anti-mouse antibodies (Mabtech) in PBS containing 0.5% FCS for 2 h at room temperature. After washing five times with PBS to remove free biotinylated anti-mouse antibodies, plates were incubated for 2 h with detection antibodies conjugated to streptavidin–alkaline phosphatase

at 1:1000 dilutions in the same buffer as above. The enzyme reaction was developed with nitroblue tetrazolium bromo-4-chloro-3-indolyl-phosphate chromogen substrate (Mabtech). The spot-forming units (SFU) per 105 cells were counted using a dissection microscope (Carl Zeiss, Stemi 2000-C). Multiscreen HTS-IP Filter Plates (96-wells, Millipore) were pre-wetted with 70% ethanol for 2 min, washed five times with

PBS and coated with 5 μg/ml of CSp in PBS Rapamycin solubility dmso overnight at 4 °C. Plates were blocked for 2 h at room temperature with complete medium. BM cells (105 cells per well) from the immunized mice were seeded in duplicates and stimulated individually with the C-CSp, N-CSp or IDE-CSp. Plates were incubated for 12 h at 37 °C, 5% CO2 and 85% humidity. After the incubation period plates were washed five times with PBS and incubated for 2 h at room temperature with HRP-conjugated goat anti-mouse IgG (1:1000; Southern Biotech) in PBS, 5% FCS. After washing with PBS five times, the reaction was developed using a Vectastain 3-amino-9-ethylcarbazole (AEC) substrate kit (Vector laboratories, Burlingame, CA) according to manufacturer’s instructions. The reactions were stopped by washing plates with deionized water. Plates were dried in the dark and spots were counted using a dissection microscope (Carl Zeiss, Stemi 2000-C). Data were analyzed using GraphPad Prism Version 5 (Graphpad Software, Inc.,

San Diego, CA). The nonparametric Kruskal–Wallis test was used for the comparison of means in different groups. For all enough tests, p ≤ 0.05 was considered significant. The combination of Ad35-CS and BCG-CS in a heterologous prime-boost regimen resulted in high-levels of CSp-specific IgG responses (Fig. 1). Moreover, antibody responses exhibited higher IgG2a (Th1-type responses) when comparing heterologous prime-boost Ad35-CS/BCG-CS to homologous prime-boost BCG-CS/BCG-CS immunizations (Fig. 1). Among the three CSp peptides tested (C-CSp, N-CSp and CSp-IDE), the response to C-CSp was synergistic and induced stronger IgG2a response in the group primed with Ad35-CS and boosted with BCG-CS (Fig. 2).

Use of plants has been reported to produce nanoparticles of variable size and shape.9 But harvesting of endangered plant species can pose a risk and imbalance in the plant diversity hence research on microorganisms as ideal source in synthesis of nanoparticles has rapidly expanded

with microorganism being isolated from various habitats and challenged with metal salts toward the unearthing nanoparticles production and this route MDV3100 research buy has gained success with large species reporting in production of nanoparticles with control size and desired shape (Table 1). The role of microbes in synthesis of nanoparticles was first reported in 1984 by employing Pseudomonas stutzeri AG259, originally isolated from silver mine. 10 Since then research on microbial synthesis of nanoparticles has expanded rapidly with one or the other reports confirming this website the production of nanoparticles by microorganism. The biological synthesis of nanoparticles originated by the experiment conducted by Mullen et al 1989 on biosorption of metals bacteria. The synthesized molecules were not identified as nanoparticles

but as aggregates. 11 Microbes produce inorganic materials either intra or extracellular often in nanoscale dimensions with exquisite morphology. Microbial interactions between metals and microbes have been exploited for various biological applications in the fields of bioremediation, biomineralization, bioleaching, and biocorrosion. The mechanism of microorganism

tolerating metal ions has led microbial system as emerging source compared to other biological entities as facile route in nanoparticle production. 12, 13 and 14 Microorganisms forms huge diversity conquering extremely hostile environments which are being bioprospected as nature wealth for wide range of application one such burgeoning area is microbes propounded as source of nanofactories with first array of microorganism being rapidly reported in synthesis of nanoparticles [Table 1] Microbial habitats forms a vital role, microbes characterized by extreme environmental conditions such as extreme pH, sparse nutrients, high metal content, intense salt load etc., are known to have unique mechanism for their existence. Marine habitat is one such resource bears a rich microbial flora with marine microorganisms these microbes are reported to have adapted toward unique mechanisms such as high salt concentration and can evade toxicity of different metal ions. Metal rich effluent is due to chemical reactions between marine water and mineral salts results in extreme environment.15 However, marine microbes acclimatize to such extreme condition for its survival. Exploiting such microbial resource for synthesis of nanoparticles will be promising enough as a facile bio-process. But reports of these microbes in synthesis nanoparticles are scanty with few reports representing the marine microbes in nanoparticles production.

These effective

antibacterial compounds may have potential to become good antibacterial drugs to treat infections caused by pyogenic bacteria. All authors have none to declare. Authors thank Dr.G.Narahari Sastry, molecular modeling group, IICT, Hyderabad for extending help pertaining to docking of the molecules and DST, New Delhi for financial support “
“Ceftibuten1 ((6R, 7R)-7-[(2Z)-2-(2-amino-1, 3-thiazol-4-yl)-4-carboxybut-2-enamido]-8-oxo-5-thia-1-azabicyclo [4.2.0] oct-2-ene-2-carboxylic acid) (Fig. 1) is a third generation cephalosporin which belongs to the class of antibiotics. It is used to treat acute bacterial exacerbations of chronic bronchitis (ABECB), acute bacterial otitis media, pharyngitis, and tonsillitis.2 Ceftibuten exerts its bactericidal action by binding to essential target proteins of the bacterial cell wall and inhibits cell-wall synthesis. It is official in Japanese Selleck OSI744 Pharmacopoeia and is selleck inhibitor assayed by High Performance Liquid Chromatography (HPLC) method. Most of the works3, 4, 5, 6, 7, 8, 9, 10 and 11 carried out includes pharmacokinetic studies of Ceftibuten in plasma and urine by HPLC and only a few spectrophotometric methods were proposed which were lacking adequate precision and accuracy. The review of literature prompted us to develop a simple, accurate, precise,

economical and rapid HPLC method for the routine analysis of Ceftibuten in bulk and capsule dosage forms in quality control labs and educational institutions. Ceftibuten Active Pharmaceutical Ingredient (API) was obtained from Aurobindo Pharma Limited, Hyderabad, India. The commercial capsule dosage formulation (Brand A) containing 400 mg of Ceftibuten was obtained from local market. HPLC grade acetonitrile (ACN), water and Adenylyl cyclase Analytical Reagent (AR) grade ammonium acetate, glacial acetic acid, ammonia was obtained from Merck Chemicals, Mumbai. Analytical Balance (Denver, M-220D), Digital pH-Meter (Labotronics, LT-11), Sonicator (Enerteck), HPLC, (Agilent, Waters 2695 separations module and 2996 diode array detector, handled by Empower2 software), analytical column-YMC-ODS, C18, 5 μ (150 mm × 4.6 mm) (YMC) were used

in present study. 15.4 g of ammonium acetate was accurately weighed and dissolved in 1000 ml of water. The pH should be adjusted to 6.7 ± 0.05, with dilute glacial acetic acid or with dilute ammonia solution and filtered. A mixture of buffer and acetonitrile in the ratio of 90:10 (%v/v) was prepared, filtered and degassed. Accurately 50 mg of Ceftibuten was weighed and transferred to a 50 ml clean, dry volumetric flask, and 30 ml of mobile was added and sonicated to dissolve. The volume was made up to the mark with the mobile phase.5 ml of this solution was taken and diluted to 50 ml with mobile phase. A series of trials were conducted using acetic acid-ammonium, phosphate and citrate buffers having different pH to obtain the required separations.

Postvaccination, seroresponse, seroprotection and hSBA GMT were all significantly higher (p < 0.001) in recipients of two doses of MenACWY-CRM than in recipients of a single dose ( Table 4 and Table 5 and Fig. 2). The purpose of this study was to assess the safety and immunogenicity of a quadrivalent vaccine, MenACWY-CRM, currently licensed for use from 11 to 55 years of age, in children 2–10 years of age in comparison with a quadrivalent vaccine (MCV4) already licensed in this younger age group. The results of the

study demonstrate that MenACWY-CRM was well tolerated and immunogenic in these young children and with a similar safety profile and favorable immunogenicity profile compared to the licensed MCV4 product. The data from this study, along with the data that supported the licensure of the vaccine in adolescents and adults, previously published data Selleck CHIR 99021 using two or three doses in the first year of life [21] and [22] and a single-dose schedule at 12 or 18 months of age [23], now demonstrate the safety and immunogenicity of MenACWY-CRM

across the age spectrum from infancy to 55 years of age. As a result of the relatively low incidence of meninogococcal disease, studies demonstrating the efficacy of new meningococcal vaccines are impractical. Instead, licensure of new GSI-IX mouse products is based on demonstrating noninferiority in the immune only response to the vaccine using immunological surrogates of protection [27]. Based on the landmark studies

of Goldschneider and colleagues in the 1960s [26], bactericidal activity at a serum dilution of 1:4 using human complement was correlated with protection against invasive meningococcal disease. More recently, Trotter and colleagues confirmed the inverse correlation of serum bactericidal titer (using rabbit serum and a threshold of 1:8) and incidence of invasive serogroup C meninogococcal disease in the United Kingdom prior to universal immunization [28]. However, given the variability observed with biological assays, many regulatory authorities prefer the use of a 1:8 threshold as a surrogate measurement of protection [29]. In contrast to seroprotection where one posits that the presence of a certain level of antibody will correlate with protection against invasive disease, comparative vaccine studies benefit from a more nuanced analysis. Seroresponse is a measure of an individual’s immune response to a meningococcal antigen that may provide a more complete comparative picture of vaccine response, including those populations with elevated baseline antibody titers. In this study, seroresponse was defined as the development of seroprotective antibody levels in individuals previously seronegative to the specific capsular antigen or a four fold or greater increase in antibody in individuals already seropositive to that antigen.