1)

(Kane and Trochim, 2007 and Trochim, 1989) We define

1)

(Kane and Trochim, 2007 and Trochim, 1989). We define key terms in Table 1. Prior to undertaking the concept mapping process, we developed a framework to identify stakeholders invested in the area of the built and social environments and older adults’ mobility (Schiller et al., 2013). We defined stakeholders as individuals and organizations with relevant interest or expertise, notably those who were either affected by or who could affect (Freeman, 1984) at least one component of the interaction between the built and social environments and older adults’ mobility. Relevant Neratinib expertise was conceptualized as employment at a relevant agency or organization, reputation within the research community as a content expert, the first-hand experience from older adults, or on recommendation as an appropriate stakeholder. We believed that all invited stakeholders would have insights into the needs of older adults so we did not restrict participation by age. Thus, based on our preliminary work developing a framework for identifying relevant individuals and organizations (Schiller et al., 2013), we recruited stakeholders from seven categories, including: policy/government; researchers; health practitioners/professionals; health and social service providers; not-for-profit organizations; private business, and older adults. Following the development of our framework, we invited two target groups: a broad group of stakeholders heavily targeting

older adults to gather their perspectives during the initial brainstorming task, and a smaller representative group of core stakeholders who participated AZD8055 concentration in both the initial brainstorming and the subsequent sorting and rating tasks (Kane and Trochim, 2007). For our older adult participants, we used an email-based recruitment strategy sent to

chapters of an organization for retired persons. To populate the other six categories of key stakeholders, we used email to invite stakeholders via known experts and Carnitine palmitoyltransferase II listservs for content area specializations and professional organization. As part of this recruitment strategy we targeted groups from the planning sector, health care sector as well as academia. We aimed for diverse perspectives to inform this project, and although responses were anonymized, we were able to capture some information on respondents (e.g., self-identified primary and secondary stakeholder group, location, occupation and age). We recruited a diverse group of stakeholders to participate; and seventy-five participants completed the brainstorming phase (including 49 participants from the broad group and 26 participants from the core group). Data from the brainstorming component were collected between May 23, 2012 and June 10, 2012. The mean age of participants was 65.1 (10.4) years (range 35–81 years); and they all resided in British Columbia, Canada, with N = 56 from Metro Vancouver, N = 10 from smaller urban centers outside of Metro Vancouver and N = 9 from rural communities.

Orally delivered vaccines have the additional challenges of survi

Orally delivered vaccines have the additional challenges of surviving the harsh gastric and intestinal environments while being present in high enough concentrations so that they are ATR inhibitor not too diluted in the intralumenal fluid of the gut [3]. This has prompted extensive research for developing mucosal adjuvants and non-replicating delivery

systems such as detoxified cholera toxin (CT) and E. coli heat labile toxin (LT), CpG-OGN, and various types of microparticulates [34], [35], [36] and [37]. Although there remain many unresolved issues related to the final clinical application of these experimental mucosal adjuvants [31], [34], [35], [36], [37] and [38], the relative success in early clinical trials of CpG-ODN as a mucosal adjuvant demonstrates the feasibility of development of effective mucosal adjuvants with acceptable side effects. The first direct evidence for the potential application of c-di-GMP as a mucosal adjuvant came from Ebensen et al. who demonstrated that i.n. co-administration of c-di-GMP with β-Gal or ovalbumin (OVA) induces efficient antigen-specific secretory

IgA production in the lung and vagina as well as cytotoxic T lymphocyte (CTL) responses [39]. When β-Gal was co-administered intranasally with c-di-GMP three times at 2-week intervals, β-Gal specific serum IgG antibody titers were significantly higher in β-Gal + c-di-GMP mice than in mice vaccinated with antigen alone. More importantly, β-Gal specific IgA titers in the lung and vaginal lavages were either significantly http://www.selleckchem.com/products/Everolimus(RAD001).html higher in mice immunized with c-di-GMP-adjuvanted β-Gal [39]. In addition to strong humoral immune responses at mucosal sites, β-Gal specific cellular immune responses were induced in spleens from mice vaccinated with β-Gal + c-di-GMP as assessed by lymphocyte proliferation. Also, i.n. immunization with OVA + c-di-GMP resulted in an in vivo CTL response (approximately 28% versus 5% specific lysis by spleens from mice immunized with OVA only) [39]. In contrast to their earlier work with systemic

immunization, which leads to a balanced Th1 and Th2 host immune response, i.n. immunization with β-Gal + c-di-GMP seems to skew the immune response toward a predominantly Th1 type as evidenced by higher serum levels of IgG2a and high IFN-γ and IL-2 secretion by splenocytes from mice immunized with β-Gal + c-di-GMP [39]. Recent work in our laboratories further demonstrated, for the first time, that the mucosal immune response induced with c-di-GMP-adjuvanted vaccine does indeed translate into protective immunity against bacterial infection [23]. We showed that i.n. immunization of mice with c-di-GMP-adjuvant pneumococcal surface adhesion A (PsaA) induces specific IgA in both the local bronchoalveolar space and distal mucosal sites (feces) as well as serum IgG1 and IgG2a responses. As was found by Ebensen et al.

However, intestinal epithelial cells have not been found infected

However, intestinal epithelial cells have not been found infected in these species and the initial target cells used by HPAIV H5N1 following intestinal inoculation are unknown. Neurons may represent candidates for initial infection, as their cellular surface harbours sialic acid with α2,3 linkage

to galactose in humans [59], allowing attachment of avian influenza viruses. Neurons are abundant in the olfactory epithelium of the upper respiratory tract, as well as in the wall of the intestinal tract. Neuronal transmission from the nasal cavity to the olfactory bulb has been demonstrated Selleck ABT-199 for HPAIV H5N1 in mice, suggesting a potential neuronal route of entry of the virus in this species [88]. In ferrets, lesion patterns in the olfactory bulb indicate similar neuronal spread of HPAIV H5N1 from the nasal cavity to the brain [89], [90] and [91]. CB-839 research buy However, no evidence of neuronal transmission initiated in the intestinal wall has been found in cats inoculated directly in the intestine, and it was suggested that these viruses may use microfold (M) cells for initial infection and entry [52]. Following virus attachment to cellular receptors, the HA protein of influenza viruses mediates the fusion of the virus and host cell membranes [53].

The HA protein needs to be cleaved into two polypeptide chains (HA1 and HA2) by host proteases to allow membrane fusion [92]. Only Non-specific serine/threonine protein kinase cleaved HA protein can undergo an irreversible conformational change triggered by the low pH of the host cell endosome that has internalized the virus, resulting in fusion of the virus envelope with the endosomal membrane. The presence of host proteases catalyzing HA cleavage is necessary at the site of virus entry to initiate infection following cross-species transmission of zoonotic influenza viruses (Table 2). The cleavage site of LPAIV HA protein is characterized by a single arginine residue, and is cleaved by extracellular trypsin-like proteases, which must be present at the portal of entry for infection with LPAIV to take place. These enzymes are present in a limited number of

host tissues, contributing to the development of a localized infection [92]. Trypsin-like proteases are abundant in the intestinal tract of birds [56] and [57]. In mammals, trypsin-like proteases have been shown to be present in the respiratory tract of swine, mice, rats and humans and can activate cleavage of influenza virus HA protein in vitro [93], [94], [95], [96], [97], [98], [99], [100], [101] and [102] (Table 3). In humans, those include the serine protease TMPRSS2, a type II transmembrane protease [103], and human airway trypsin-like proteases (HAT), which occur in both transmembrane and soluble forms [99] and [100]. The role these enzymes play in vivo during infection with influenza virus of zoonotic or human host origin is not known.

The AUC0–t was obtained by the trapezoidal method AUC0–∞ was cal

The AUC0–t was obtained by the trapezoidal method. AUC0–∞ was calculated up to the click here last measureable concentration and extrapolations were obtained using the last measureable concentration and the terminal elimination rate constant (Ke). The terminal elimination rate constant (Ke), was estimated from the slope of the terminal exponential phase of the plasma of Acamprosate concentration-time curve (by means of the linear regression method). The terminal elimination half-life t1/2 was then calculated as 0.693/Ke. Regarding AUC0–t, AUC0–∞ and Cmax

bioequivalence was assessed by means of analysis of variance (ANOVA) and calculating the standard 90% confidence intervals (90% CIs) of the ratios test/reference (logarithmically transformed data). The bioequivalence was considered when the ratio of averages of log transformed data was within 80–125%

for AUC0–t, AUC0–∞ and Cmax. 14 and 15 Mass parameters optimization, chromatography optimization, suitable extraction method optimization to be optimized during method development, prior to validate the method. During mass parameters optimization, type of ionization is important to get the respective parent and product ions. In our case, Electrospray ionization (ESI) was chosen as ionization technique. In ESI mode, compound dependent parameters (DP, EP, FP, CE, CXP) and source dependent parameters (CUR,CAD, Heatergas, nebulizer gas) temperature, voltage conditions were optimized to get better signal and response of the analyte and internal standard. Acamprosate Palbociclib cell line gave more response in negative ion mode as compare to the positive ion mode. The predominant

peaks in the primary ESI spectra of Acamprosate and Acamprosate D12 corresponds to the MH-ions at m/z 180.0 and 186.1 respectively ( Figs. 2a, 3a). Product ions of Acamprosate and Acamprosate D12 scanned in quadrupole 3 after a collision with nitrogen in quadrupole 2 had an m/z of 79.91 and 79.9 respectively [ Figs. 2b, 3b]. During chromatographic Histone demethylase optimization, selection of suitable mobile phase and suitable column are the primary aspects. Mobile phase containing ammonium acetate and acetonitrile in varying combinations was tried, but a low response was observed. Further, it was changed to acetic acid: acetonitrile (20:80 v/v) and acetic acid: methanol (20:80 v/v) observed bad peak shape. After that, mobile phase containing 0.1% formic acid in water in combination with methanol and acetonitrile with varying combinations were tried. Using a mobile phase containing 10 mM ammonium formate (Ph: 3.5): acetonitrile (10:90 v/v), the best signal along with a marked improvement in the peak shape was observed for Acamprosate and Acamprosate D12. Different columns like, symmetry shield RP18 (50 × 2.1 mm, 3.5 μm), Inertsil ODS-2V (50 × 4.6 mm, 5 μm), Hypurity C18 (50 × 4.6 mm, 5 μm) and Hypurity Advance (50 × 4.0 mm, 5 μm) were used in the method development.

Therefore, we believe that DIM may be a potential prophylactic an

Therefore, we believe that DIM may be a potential prophylactic and/or therapeutic agent for bone diseases, such as postmenopausal osteoporosis. The authors indicated no potential conflicts of interest. We would like to thank Dr. Y. Imai for his technical support and advice. This work was supported by a postdoctoral fellowship for foreign researchers (Grant number 12F02106 to TY) from the Japan Society for the Promotion of Science (JSPS). “
“Colorectal cancer (CRC) is one of the most common cancers and a leading cause of cancer death in both men and women. Although promising progress

has been made in the diagnosis and treatment of CRC over the last decade, this CB-839 concentration cancer remains a major public health problem (1), (2) and (3). There is an urgent demand to better understand the molecular mechanisms underlying the different phenotypes of CRC. This understanding may provide information supporting drug discovery and prevention strategies (1). The development of human genome technologies, such as DNA microarrays, has allowed us to simultaneously examine thousands of genes, leading to a better understanding of carcinogenesis (4). Studies related to compound treatment outcomes by differences in gene expression profiling facilitate the search for more curative interventions buy PFT�� (5). Increasing evidence shows that patients with cancer often resort to complementary

and alternative medical supplements to treat cancer, cancer-related symptoms, or to reduce the adverse effects of chemotherapy (6). Botanicals can contain effective anticancer compounds Edoxaban that can be used alone or as

adjuncts to existing chemotherapy, thereby improving efficacy and reducing drug-induced adverse events (7) and (8). In current cancer treatment, approximately 80% of novel drugs have originated from natural products (9). American ginseng (Panax quinquefolius L.) is a commonly used herbal medicine in the United States. Protopanaxadiol (PPD, Fig. 1), an aglycon of ginseng saponins from the ginseng, has shown anticancer potential in our previous studies (10). However, the previous study emphasized in vitro bioactivity screening using PPD and its derivatives, the in vivo antitumor effects were not evaluated. In addition, PPD’s anti-CRC mechanisms have largely not been explored. To better understand the anticancer effects of PPD, in the present study, we first used an athymic nude mouse xenograft tumor model to observe the compound’s in vivo activity. Next, a panel of human colorectal cancer cell lines (i.e., SW-480, HT-29, and HCT-116), which differ in the expression of the tumor suppressor gene, p53, were used to compare the anti-proliferation activities. Then, HCT-116 cells, which showed the most significant growth inhibition by PPD, were selected to explore the compound’s effect on mRNA.

Also, inflammation scores in brain tissues after parasite challen

Also, inflammation scores in brain tissues after parasite challenge predominated in mice immunized with NLA + ArtinM and ArtinM alone. These findings are likely associated with the enhanced IFN-γ/IL-10 and IgG2a/IgG1 ratios after parasite challenge observed in these animals, reflecting in a Th1-type biased pro-inflammatory immune

response induced in the acute phase of the infection. It is well known the role of T CD4+ cells and mostly IFN-γ to control N. caninum infection [6]. On the other hand, the induction of a type 2 immune response associated with a pattern of anti-inflammatory response is not protective to neosporois [41]. Therefore, we believe that a non-exacerbated pro-inflammatory immune response is associated with the host resistance to parasite infection and consequently the progression to the asymptomatic chronic phase of neosporosis. Accordingly, in our experimental check details design, the induction of a pro-inflammatory immune response by ArtinM associated with NLA showed to be beneficial rather than deleterious to the host to control neosporosis. A previous study also showed that the combination of ArtinM with soluble Leishmania antigen (SLA) induced IFN-γ production, thus reducing the parasite load, but without decreasing the lesion size [16]. Interestingly, in the present study,

the survival curves showed deaths occurring earlier PLX3397 solubility dmso than our previous report [29], although we have used the same mouse lineage and the same Histone demethylase tachyzoite number (2 × 107 tachyzoites/mouse) for challenge. An explanation for these findings is likely because we employed in the present study a N. caninum isolate from lower passage than that used in our previous study. Accordingly, it is known that long-term passage of tachyzoites in tissue culture can attenuate virulence of N. caninum in vivo [32]. On the other hand, mice immunized with NLA + JAC or NLA alone presented an anti-inflammatory or immunoregulatory profile, leading to higher parasite burden, suggesting that

the immune response induced in these groups was not effective. In contrast, a previous study evaluating the adjuvant effect of Jacalin associated with epimastigote forms of T. cruzi showed that the parasite load of mice immunized was reduced after challenge with trypomastigotes in relation to the group immunized with parasite alone [14]. Surprisingly, mice immunized with the ArtinM lectin alone showed the lowest brain parasite load compared to the other groups, although with no significant difference to the NLA + ArtinM group. This finding associated with enhanced IgG2a/IgG1 ratio after parasite challenge and increased IFN-γ/IL-10 ratio observed in ArtinM group, may indicate that the immune stimulating effect of the ArtinM lectin itself may be a good target for therapies and it can stimulate an innate immune response dependent of the Toll-like 2 receptor for production of IL-12.

However, the IgA analysis lacked a control group and thus it is d

However, the IgA analysis lacked a control group and thus it is difficult to interpret the high observed response. Based on the detection of increased influenza-specific IgG and IgA circulating antibody-secreting B cells 1–2 weeks

following LAIV vaccination with minimal subsequent increases in serum antibody and systemic memory B cells, Sasaki et al. proposed that LAIV provides protective immunity through a local B-cell memory Selleck SB203580 response in the upper respiratory tract [26]. This mechanism is consistent with the current analysis and represents a plausible explanation of LAIV-induced antibody-mediated immunity, which is critical to block influenza virus infection [1]. However, it is clear that other aspects of the immune system contribute to LAIV-induced protection from influenza. In the current analysis and in a study by Boyce et al., the highest IgA responses were directed against the B strains followed by A/H3N2 [27]; however, LAIV has demonstrated similar and high efficacy in children against all 3 types/subtypes [11] and [37]. Studies have demonstrated that LAIV-induced immunity

can also be partially explained by T-cell immunity [17], [28], [29] and [38] and serum antibody responses [39]. Stimulation of innate immunity via interferon and natural killer cells may also contribute to LAIV-induced protection, particularly when influenza circulates shortly after vaccination [38], [40], [41] and [42]. As an attenuated live DNA Damage inhibitor virus vaccine, it would be expected that LAIV would induce a multi-faceted immune response, similar to that induced by wild-type influenza infection and other live virus vaccines [1]. It is likely that no single component of the response can fully explain the protective and effect induced by LAIV. Under the classification of correlates of protection for vaccination proposed by Plotkin [43] and [44], the association between LAIV-induced

protection and measured IgA responses would be best classified as a relative co-correlate of protection. The relative co-correlate classification is appropriate because strain-specific IgA responses were associated with protection in LAIV recipients, but the level of response observed varied by strain and study and vaccine-induced protection has been shown to be correlated with other components of the immune response. Additionally, it is worth noting that no relationship between strain-specific IgA ratios and influenza illness incidence was observed among placebo recipients, which is a requirement for a more robust correlate of protection [43] and [44]. However, this lack of an association among placebo recipients is likely due to limited baseline strain-specific anti-influenza mucosal immunity among the study subjects given their young age.

It adds to the growing diversity of opinion of the hypothesised m

It adds to the growing diversity of opinion of the hypothesised mechanisms of motor control in LBP. This is an important reminder that there should be a separation between the research question asking if the treatment works, and how or why the treatment works. Too many therapists and researchers rely on one to justify the other. “
“The Western Ontario Rotator Cuff Index (WORC) is a condition-specific self-reported instrument to assess ‘quality of life’ (QoL) (Kirkley et al 2003). It consists of 21 visual analog scale (VAS)

items organised in 5 subscales: physical symptoms, sports/recreation, work, lifestyle, and emotions. It was developed by a clinimetric Ruxolitinib chemical structure process. The origins of the subscale structure were not established Dasatinib price by a factor analysis; and are

similar to those contained on instruments developed by the same author for other shoulder conditions (osteoarthritis and instability) (Lo et al 2001). The WORC has been translated and validated in several languages. Instructions to client and scoring: Patients are asked to indicate on a 100-mm line, anchored at the beginning and at the end, the extent to which the symptom or disability is experienced over the past week referring to the problematic shoulder. Phrases like ‘no pain’ and ‘extreme pain’, ‘no weakness’ and ‘extreme weakness’, ‘no difficulty’ and ‘extreme difficulty’ which explained the extremes of a particular item measured, were used as anchors. Each item in WORC has a possible score from 0–100 (100 mm VAS). Scores can be computed for individual subscales and summated for a total score, which can range from 0–2100, with a higher score representing lower quality of life. To present this in a more clinically meaningful format, the distance from the left side of the line is measured and recorded to the nearest 0.5 mm, calculated for a score of out of 100, and summed for each subscale (physical

symptoms/600, sports and recreation/400, work/400, lifestyle/400, and emotions/400). not The subscale scores are summed and reported as a percentage of normal by subtracting the total from 2100, dividing by 2100, and multiplying by 100 (Kirkley et al 2003). Reliability, validity and responsiveness: The WORC has demonstrated good test-retest reliability across several studies (ICCs 0.84 to 0.96) (Kirkley et al 2003, Ekeberg et al 2008, de Witte et al 2012). The construct validity of WORC as determined by comparison to other disability instruments has been supported (Longo et al 2011). The WORC correlates with the American Shoulder and Elbow Surgeons score (ASES) (r = 0.68) and the Disabilities of the arm, shoulder and hand (DASH) (r = 0.63) (Kirkley et al 2003). Factor validity of the 5-domain structure of WORC has been questioned. In one study 3 factors (symptoms and emotional items, strength items, daily activities) were identified representing 57% of variance (Wessel et al 2005).

To examine if FomA contributes to the co-aggregation of F nuclea

To examine if FomA contributes to the co-aggregation of F. nucleatum with P. gingivalis, we first generated neutralizing antibody to FomA via immunization of ICR mice with E. coli-based vaccines

[25]. The gene encoding FomA was amplified by PCR using specific primers and genomic DNA prepared from F. nucleatum. The PCR products were inserted into a pEcoli-6×HN plasmid and expressed in E. coli [E. coli BL21(DE3)]. After IPTG induction, the over-expressed FomA-6×HN fusion protein at approximately 40 kDa molecular weight was detected by SDS-PAGE with coomassie blue staining ( Fig. 2A). FomA ( Fig. 2B) was purified using a nickel–nitroloacetic acid column. Twenty-eight internal peptides ( Supplementary Fasudil molecular weight Table 1) derived from expressed FomA were fully sequenced by Nano-LC–LTQ-MS analysis after in-gel trypsin digestion, matching well with those from F. nucleatum FomA (GenBank Accession Sunitinib manufacturer Number: gi|19713103). An internal peptide (VVEYVEKPVIVYR; 34–46 amino acid residues) of FomA is presented ( Fig. 2C), validating the expression of recombinant

FomA. Next, a vaccine was constructed using inactivated whole E. coli particles over-expressing FomA. To assess the immunogenicity of FomA, ICR mice were vaccinated with UV-inactivated-E. coli over-expressing FomA or a negative GFP control protein [E. coli BL21(DE3) FomA or GFP] for 9 weeks. A strong band appearing at approximately 40 kDa was visualized when purified FomA was reacted with the serum obtained from mice immunized with [E. coli BL21(DE3) FomA], demonstrating the immunogenicity of FomA ( Fig. 3A). No immunoreactivity against FomA was detected when serum from mice immunized with [E. coli BL21(DE3) GFP] were used. To examine if FomA participates in bacterial co-aggregation and biofilms, F. nucleatum was neutralized with serum from mice immunized with [E. coli BL21(DE3) FomA] (anti-FomA serum) and then incubated in the presence or absence of P. gingivalis. Neutralization with serum from mice immunized with [E. coli BL21(DE3) GFP] (anti-GFP serum) served as a control. As shown in Fig. 3B, the co-aggregation of anti-GFP serum-neutralized F. nucleatum

with P. gingivalis generated a peak signal ranging from 825 to 1718 nm on the spectrum of Zetasizer Nano-ZS. The size of aggregate was decreased to 458–825 nm ( Fig. 3B) when P. gingivalis was many mixed with F. nucleatum neutralized with anti-FomA serum. Similarly, biofilm enhancement was detectable, as expected, in a co-culture of P. gingivalis with F. nucleatum neutralized with anti-GFP serum. However, the enhancement was dramatically abrogated when anti-FomA serum-neutralized F. nucleatum was co-cultured with P. gingivalis ( Fig. 3C). These results indicate that a neutralizing antibody to FomA was produced after immunization and confirmed that FomA mediated the co-aggregation and biofilm formation of F. nucleatum with P. gingivalis. We previously determined that co-injection of F.

This complemented the original 2006 Roadmap strategic goal

This complemented the original 2006 Roadmap strategic goal DAPT molecular weight of developing a highly efficacious vaccine to prevent clinical disease [2] and highlighted the definitive shift of the broader malaria community to a focus on the development of tools to accelerate elimination and eventual eradication of malaria. The leadership of the Bill & Melinda Gates Foundation (Gates Foundation), along with the World Health Organization (WHO), the Roll Back Malaria Partnership, and other key stakeholders, have challenged the malaria community to renew its efforts

to eradicate malaria [3], therefore leading to a significant refocusing of associated product development efforts [4]. Over the last several years, as the malaria community began to embrace the challenge of eradication, questions arose about the feasibility of such an endeavor, the tools and strategies that would enable it, and the gaps that would need to be addressed in order to support eradication as a long-term goal. A number of meetings and consultations took place in and around 2010 to define the research agenda for malaria eradication, including those associated with the development of a malaria vaccine to interrupt malaria (parasite) transmission SB431542 research buy (VIMT) [5], [6], [7], [8], [9], [10], [11],

[12], [13], [14], [15] and [16]. Initially P. falciparum and P. vivax were prioritized, with the recognition that to truly eradicate malaria, all species that infect humans must eventually be addressed. This article describes the progress that has since been made in critical focus areas identified Non-specific serine/threonine protein kinase during those meetings (Clinical development pathway and regulatory strategy; Assays; Transmission measures and epidemiology; Communications and ethics; Policy and access; Process development and manufacture; specific challenges associated with targeting P. vivax), and highlights the next steps that will be critical to developing the classes of vaccines needed to support the community’s malaria-eradication goals, as laid out in the revised Roadmap. While vaccines have the potential to interrupt malaria transmission at multiple points in the parasite

lifecycle, this paper will focus on strategies targeting the sexual, sporogonic, and mosquito (SSM) stages of the parasite (hereafter referred to as an SSM-VIMT), which are involved in the transmission of malaria parasites from an infected person to a female mosquito, rather than those involved in parasite infection of the human host or causing malaria disease. While not a novel concept, as evidenced by the 2000 meeting report on transmission-blocking vaccines (TBVs), “an ideal public good” [17], the product development resources now available to apply to the development of such products have created significant new opportunities. Unique development challenges associated with this class of VIMT, most notably the delayed as opposed to immediate benefit conferred to immunized individuals, require special consideration.