The

mechanisms underlying this potential relative resistance to post-teriparatide bone loss in men are unclear. This observation requires confirmation in larger studies and in men and women receiving the approved teriparatide dose of 20 mcg/day. One concern is that teriparatide appears to require continued administration for a sustained biological effect, unlike bisphosphonates that have persistent effects on bone resorption many months after drug exposure [75], [76] and [77]. However, Lindsay et al. also reported that women with postmenopausal osteoporosis showed sustained vertebral fracture risk reduction after withdrawal of teriparatide (at least 18 months) [73]. Finally, a post-marketing study on the use of teriparatide in the US, derived check details from the Direct Assessment of Nonvertebral Fracture in the Community Experience (DANCE) study, described gender differences for initiating teriparatide therapy. The drug was used more often in women, based

on general frailty, low body mass and an inadequate response or intolerance to previous therapy. Chronic glucocorticoid therapy was the reason most often given by investigators for initiating therapy in men, and more often used as an indicator for therapy in men, illustrating the possibility that at least in the US, physicians view teriparatide use somewhat differently in men vs. women [78], and providing further evidence from a clinical practice setting that male osteoporosis is under-diagnosed and likely under-treated. A study randomly assigned 83 men with low BMD to receive 10 mg/day alendronate, 40 mcg/day teriparatide subcutaneously, or both. Alendronate was administered for 30 months, Fluorouracil ic50 and teriparatide was started after six months. Lumbar spine and femoral neck BMD increased significantly more in men on teriparatide monotherapy compared with the other groups. Changes in serum BTM were significantly greater in the teriparatide group than in the alendronate group or

the combination therapy group (p < 0.001). As with BMD, a second study showed that alendronate impaired the action of teriparatide to increase bone turnover in men [79] and [80]. Previous studies in postmenopausal women also suggested that concomitant alendronate Palbociclib concentration and PTH (1–84) reduced the anabolic effects of PTH [75] and [81]. These data may influence therapeutic choices after PTH discontinuation, because its use is limited to a maximum of two years [75]. Although these studies suggested that combination of teriparatide and bisphosphonates had no additive effect because alendronate diminished the teriparatide effect, zoledronic acid was shown not to block the anabolic effect of PTH. In a one-year partial double-blind randomised study of 412 postmenopausal women, Cosman et al. concluded that, while teriparatide increased spine BMD more than zoledronic acid, and zoledronic acid increased hip BMD more than teriparatide, combination therapy provided the best BMD improvement, both in spine and hip BMD [82].

Under real conditions in the immediate vicinity of a coastline, waves

run up and down the beach surface. Let us consider first the function of mean sea level elevation when the only parameter dependent on the external TGF-beta inhibitor factors is the parameter γ=Hhbr. When α = − 1, from (20), we obtain the following approximate relationship: equation(22) Hx=Hhbrhx=γbrhx. In practice, the value of parameter γbr ≈ 0.7 − 0.8. By substituting (22) in formula (14) we obtain: equation(23) Sxx≈316ρgγbr2h+ζ¯2. In the general case, the elevation of the mean sea level set-up ζ¯x is not a linear function of x. Note that if instead of equation we assume relation  (20), the solution of equation (13) results in a nonlinear (as a function of distance) variability of the mean sea level elevation ( Dally et al. 1985): equation(24) dζ¯xdx=−3161hx+ζ¯xdH2xdx2. Figure 3 compares the mean sea level elevation set-up using the linear approximation (relation 17) and the nonlinear approximation (24). During a controlled large-scale laboratory experiment carried out in the Large Wave Channel in Hannover, a data this website set was gathered which compares better with the nonlinear set-up (Massel et al. 2005). The distance shown on the horizontal axis is the distance in metres for coastal areas, reflected by the beach heaped up in the GWK laboratory in Hannover (Figure 4),

where initially, the bottom was flat. Re-profiling into the bottom at an angle β = 1/20 starts at the point of 150 [m] from the beginning of the channel laboratory, and 230 [m] is the point of intersection of the sea water level with the seabed. ‘0’ is beginning of the wave channel, the point where waves

are generated. This notation has been retained to maintain consistency with the work by Massel et al. (2004). Elevation of the mean sea level is dependent on the characteristics aminophylline of the wave arriving from the open sea. Let us consider, therefore, changes in the mean sea level elevation during during several hours of a storm. Let us assume that as storm waves approach the costal zone, their height H0(t) changes over deep water according to the following formula: equation(25) H0t=1+cos2πt24−12+H0t0, where the height H0(t0) = 0.3 [m]. Let the wave period T = 6 [s] and the bottom slope β = 1/20 the duration of the storm is 24 hours. Depending on the height of the wave approaching the shore, the width of the surf zone changes. Figure 5 shows the changes of H0(t) in time during a 24-hour storm. The narrow strip of sea, along the coast, between depth Hbr, where the wave begins to break, and the shoreline is the surf zone. The experiment of Singamsetti & Wind (1980) shows that the depth at the breaking point Hbr, the breaking wave height Hbr and the value γbrnoindent are expressed by the following formulas: equation(26) Hbr=0.575β0.031H0tL0t−0.254H0t, equation(27) Hhbr=0.937β0.155H0tL0t−0.130, equation(28) hbr=0.614β−0.124H0tL0t−0.

The advantage of our non-hydrostatic model over widely used non-dispersive shallow water models is that it can be used to capture wave dispersion

by including multiple vertical layers (Oishi et al., 2013, e.g.), MAPK inhibitor but can also approximate the shallow water approach using a single layer to model the propagation of non-dispersive waves (Mitchell et al., 2010, e.g.). As the slide-tsunami scenarios we investigate here generate non-dispersive or very weakly dispersive waves our simulations generally use only a single layer. While this results in a (modest) computational overhead compared to alternative formulations, the benefit is that the results presented here can be directly compared with future

studies, using the same model, that examine highly dispersive waves generated by, for example, smaller slides SP600125 solubility dmso (Glimsdal et al., 2013, e.g.). Mitchell et al. (2010) used the same model to study ancient tsunamis in the Jurassic Tethys sea, which shows the flexibility of the model in representing arbitrary coastlines. Here we describe how Fluidity has been modified to simulate slide-tsunami generation using prescribed rigid-block slide motion. This allows two of the four phases of slide-generated tsunami waves to be studied (Harbitz et al., 2006): the generation and propagation of the wave. The simulation of slide dynamics and tsunami wave inundation are not considered in this work. Previous studies of the Storegga slide tsunami did not directly include the effects of relative sea-level changes on bathymetry (Harbitz, 1992 and Bondevik et al., 2005). Isostatic adjustments from ice-sheet loading and unloading produce complex changes in relative sea-level across the region. Recent studies have simulated this process to produce 1000-year time slices of such changes since the Last Glacial Maximum (Bradley et al., 2011). Relative sea-level changes of up to 50 m have occurred since the Storegga slide, Rebamipide which caused substantial changes in

coastlines. For example, 8000 years ago a region in the southern North Sea was an island—Doggerland (Fitch et al., 2005)—and the coastlines around Norfolk, UK, and the northern coast of mainland Europe (Fig. 1) were dramatically different. Human artefacts (flints and spearheads) and mammal remains (mammoth and rhinoceros teeth) have been dredged from the Dogger Bank (Flemming, 2002). There has been speculation that the Storegga tsunami was the cause of the abandonment of the island by Mesolithic tribes (Weninger et al., 2008). In this paper, we first briefly describe the Fluidity model and the newly-implemented rigid-block slide model used to initiate the tsunami. We verify the implementation of this model by comparing our results to previous numerical results for test problems in both 2- and 3-dimensions.

Biglycan also plays a role in organizing membrane architecture and function in muscle and at synapses. Raf inhibitor Muscle membranes are highly specialized to transmit force, protect the cell from contraction-induced damage and orchestrate signaling pathways required for normal function. The dystrophin-membrane and utrophin-membrane glycoprotein complexes (DGC and UGC, respectively) link the cytoskeleton to the extracellular matrix and serve as a scaffold for signaling molecules in adult (DGC) and immature (UGC) muscle. Biglycan binds to three

shared components of these complexes: the extracellular peripheral membrane protein α-dystroglycan and the transmembrane proteins α-sarcoglycan and γ-sarcoglycan [6 and 7]. Genetic studies show that biglycan regulates the expression of utrophin, the two sarcoglycans and an intracellular membrane-associated signaling complex comprised of dystrobrevin, syntrophins and nNOS (neuronal nitric oxide synthase) in immature muscle [8]. Notably, dosing mice with recombinant non-glycanated biglycan (rNG-BGN) can restore the expression

of several of these components to the membrane [8]. The role of biglycan in binding and regulating several components of DGC and UGC, coupled with the ability to deliver rNG-BGN systemically, suggested that biglycan could be a therapeutic for Duchenne Muscular Dystrophy (DMD). DMD is the most common form of muscular dystrophy and results from mutations in dystrophin – a large www.selleckchem.com/products/byl719.html intracellular protein that links the actin cytoskeleton to the membrane and anchors the DGC. Notably, utrophin upregulation can compensate for dystrophin loss in mouse

models of DMD (mdx; Davies). Systemically delivered rNG-BGN recruits utrophin to the membrane and improves muscle health and function in mdx mice [9]. The efficacy of the non-glycanated form (i.e. lacking GAG side chains) in this therapeutic approach is most probably based on two reasons. First, this form can be readily manufactured in a homogeneous form. Second, biglycan proteoglycan (PG) but not non-glycanated (core) is proinflammatory Urocanase [10]. A non-glycanated form of biglycan is currently in preclinical development for DMD. Biglycan is also important for synapse stabilization [11]. In biglycan-deficient mice, neuromuscular junctions form normally but then they become unstable about three weeks after birth. The mechanism of biglycan action at the synapses is likely to involve MuSK, a receptor tyrosine kinase that is the master regulator of synapse differentiation and maintenance. Biglycan binds to MuSK and regulates its expression in vivo. Notably, synaptic loss is one of the earliest abnormalities observed in almost all neurodegenerative diseases, including ALS (amyotrophic lateral sclerosis) and SMA (spinal muscular atrophy).

6 μg/L Dabrafenib order (IR3535®1) and 0.4 μg/L (IR3535®-free acid 2), respectively. The kinetics of excretion of IR3535®1 and IR3535®-free acid 2 is shown in Fig. 5. Concentrations of parent IR3535®1 in urine were very low (more then 4 orders of magnitude lower than those of IR3535®-free acid 2) as expected from the rapid metabolism to IR3535®-free acid 2. Peak concentrations of IR3535®1 and IR3535®-free acid 2 were observed in urine samples at the first two collection points four and eight hours after dermal application of IR3535®1 (Fig. 5). Excretion of IR3535®-free acid 2 declined rapidly to reach concentrations close to the LOQ 48 h after application, half-life of urinary excretion

was approx. six hours. Only 2.9 μmoles of IR3535®-free acid 2 were excreted in the time interval between 36 and 48 h after dermal application of IR3535®. Based on the total amount of IR3535®1 and IR3535®-free acid 2 excreted in urine, the extent of absorption of IR3535® after dermal application is 13.3% (Table 7). This study used a realistic exposure scenario since the chemical under study was applied to the skin as expected under typical use patterns see more in humans. The results thus give information on systemic doses received.

Therefore, due to the large amounts of applied, 14C-labeled IR3535® could not be used. Based on urinary recovery and kinetics of excretion, IR3535®1 is rapidly metabolized in humans and the resulting metabolite, IR3535®-free acid 2, formed by ester cleavage,

is rapidly excreted. The formation of IR3535®-free acid 2 as the only metabolite of IR3535®1 is well characterized and has been studied in vitro and in vivo using radiolabeled IR3535®1, which was rapidly and 3-oxoacyl-(acyl-carrier-protein) reductase completely metabolized by hepatocytes of rats and humans resulting in IR3535®-free acid 2 as the only metabolite. IR3535®-free acid 2 itself was not further metabolized ( Ladstetter, 1996). In addition, IR3535®-free acid 2 was the only metabolite detected in several animal species treated with 14C-labeled IR3535®1 orally and/or topically ( Arcelin and Stegehuis, 1996, Ladstetter, 1996 and van Dijk, 1996). Only very low amounts of non metabolized IR3535®1 were found in urine and in plasma samples suggesting intensive biotransformation as already shown in the toxicokinetics studies with IR3535® in experimental animals. The IR3535®-free acid 2 is also expected as the only metabolite of IR3535®1 in humans, since other metabolic pathways are unlikely considering the structure of IR3535®1. Unspecific esterases are present in skin, in erythrocytes and in plasma of humans ( Baron and Merk, 2001 and Parkinson and Ogilvie, 2008); therefore, most of the absorbed IR3535® is rapidly metabolized explaining the very low blood levels observed in this study.

This report provides new knowledge of endocytosis and exocytosis, as well as of BoNT trafficking and action. In particular, the results showing the efficacy of DDV-Mas-7 in rescuing neurons from botulism is consistent with our previous reports on a PLA2- and RhoB-mediated mechanism of BoNT/A toxicity. In addition, these results

suggest an alternative approach towards botulism intervention click here other than the one commonly emphasized, i.e., protection of vesicle fusion proteins, e.g., SNAP-25 for BoNT/A. “
“The simple and cost-effective preparation of proteins is an essential prerequisite for initial studies to be made to clarify the molecular mechanisms of action for many toxins. In this context, cell-free protein synthesis has emerged as a powerful technology

platform to overcome the limitations of cellular systems for the synthesis and functional characterization of proteinogenic toxins (Orth et al., 2011). The characterization of bacterial pore-forming proteins in particular, is often hampered by their potent toxicity, which prevents their expression as a recombinant protein in living cells. Such pore-forming toxins are major virulence factors of Vibrio parahaemolyticus, a halophilic bacterium inhabiting marine environments worldwide. Seafood contaminated with V. parahaemolyticus can cause diarrheal diseases in humans after ingestion of undercooked or raw seafood and has been recognized as a cause of diarrheal diseases worldwide, most common in Asia and the United States of America ( Anonymous, 2011). Most clinical strains of V. parahaemolyticus show β-hemolysis of human erythrocytes on a special blood agar (Wagatsuma agar) Selumetinib chemical structure designated as Kanagawa phenomenon (KP) ( Taniguchi et al., 1985). The KP is caused by a secreted hemolysin which has been termed thermostable direct hemolysin (TDH) because of its physicochemical properties ( Fukui et al., 2005). Strains harboring tdh genes and/or genes encoding a TDH

related hemolysin (TRH) are designated to be pathogenic, Methocarbamol while V. parahaemolyticus lacking these genes are regarded as non-pathogenic ( Nishibuchi and Kaper, 1995 and Anonymous, 2011). Biochemical and biological studies have shown that TDH is the major virulence factor of V. parahaemolyticus with multiple biological activities including hemolysis, enterotoxicity, cardiotoxicity and cytotoxicity ( Nair et al., 2007). TDH is a tetrameric toxin composed of four identical protein subunits and forms pores in eukaryotic cell membranes (Hamada et al., 2007). Genetic analysis revealed that tdh genes show slight differences in various strains of V. parahaemolyticus ( Baba et al., 1992), however, the identity of the TDH protein subunits among all different strains is above 97%. All tdh genes encode a preprotein of 189 amino acids (aa), which is secreted through the bacterial cell wall by removing a signal peptide of 24 aa at the N-terminal end.

Analyses are based on 499 children with complete DXA data at BAY 73-4506 chemical structure 6 years. Table 1 summarises the characteristics of the children. Despite similar height and weight at age 6 years, there were differences in bone indices by gender. Additionally, girls had a greater mean total fat mass compared with the boys (p < 0.0001). 395 children were of normal weight (equivalent to adult BMI < 25 kg/m2), 50 were overweight (equivalent to adult BMI between 25 and 30 kg/m2)

and 17 were obese (equivalent to adult BMI > 30 kg/m2). All, apart from 18 children were of white Caucasian ethnicity. There was no difference in the anthropometric measures at birth and at age 1 year between those children who did or did not participate in this study; however study participants’ mothers tended to be of higher social class (p = 0.004) and were less likely to smoke (p = 0.03). The subgroup of children who underwent pQCT were slightly younger than the overall group who underwent DXA (6.5 years versus 6.6 years in the overall DXA group, p < 0.01), but otherwise were broadly similar. Table 2

summarises the relationships between body composition and bone indices. Both total fat mass and total lean mass were positively associated with whole body minus head BA, BMC and aBMD. When lean mass was included in regression models, these relationships were somewhat attenuated, TSA HDAC in vitro but remained statistically significant; the associations between fat mass and bone indices

at the lumbar spine became non-significant after inclusion of lean mass. There was evidence of gender differences in the relationships between lean adjusted fat mass and the bone outcomes, which were stronger in male than female children (p value for the lean adjusted fat mass–gender interaction terms with whole body BA, BMC, aBMD all < 0.05). Similar gender differences were observed in the associations between lean-adjusted fat mass and bone indices at the lumbar spine. The results from the subgroup of 132 children who had pQCT data available for the tibia are shown in Table 3. There was a negative relationship between total fat mass and cortical density and a suggestion Diflunisal of a negative association with trabecular density. After adjustment for lean mass, total fat was negatively associated with both trabecular and cortical density. Fat mass adjusted for lean mass was associated positively with total and cortical area but not cortical thickness or stress–strain index at the 38% site. When the pQCT outcomes were adjusted for the height of the child at six years, the relationships were broadly similar, but the association between total fat and total area at the 4% site became attenuated (unadjusted β = 26 mm2/sd vs adjusted β = 7 mm2/sd) and statistically non-significant (p = 0.3).

Results of in

vitro-fertilized embryo survival following cryopreservation have been inconsistent among studies PKC inhibitor review [26], [34] and [10] and vitrification procedures for in vitro-produced bovine embryos still need improvement in order to reduce injuries to the embryos [21] and [11]. In the current study we observed that vitrification can also alter gene expression in bovine embryos produced in vitro. The lowest relative amount of Aqp3 transcripts in the vitrified-warmed embryos reported in the current study might be due to the low capacity of embryo genome in reestablishing Aqp3 transcripts store after vitrification procedures. Such disturb may suggest that despite the re-expansion and in vitro survival at 72 h after warming, vitrified-warmed embryos may undergo molecular alterations that compromise the further development. For instance, expression of Aqp3 gene and protein seems to be important to preserve homeostasis during pregnancy [2] and its deregulation may be associated to oligohydramnio in humans [41]. Therefore, alterations on expression of genes important for conception and gestation maintenance, like Aqp3, could contribute to inconsistent survival and pregnancy rates of vitrified-warmed

bovine embryos produced by in vitro fertilization. In conclusion, embryo ability to undergo shrinkage and swelling is influenced by medium used in a co-culture system and by embryo stage; therefore such aspects may be involved in cryopreservation efficiency Etomidate and should be taking into account. Vitrification can Epigenetics Compound Library datasheet alter gene expression of in vitro-fertilized bovine embryos co-cultured with cumulus cells but the expression of Aqp3 and Na/K ATPase1 genes seems to be not associated to rehydration of bovine embryos challenged

with NaCl hypertonic solution. The authors thank to M.P. Palhao for his assistance on figures and graphs edition and B.C. Carvalho and M.M. Pereira for assistance on embryo cryopreservation. MC Boite was supported by CAPES foundation. This study was supported by CNPq project No. 471517, Fapemig project No. CAG1217-05 and Embrapa MP1 01.07.01.002.05. “
“Just over 60 years have passed since the first successful experiment on freezing goat sperm [34]. In spite of all this time, protocols for goat semen cryopreservation continue to be developed due to the wide range of results found for sperm motility, considered the parameter of choice to determine the degree of sperm damage inflicted by the cryopreservation procedure [3], [9], [18] and [19]. These results have varied from low values as 6% up to 62%, being the last reached with the use of antioxidants into the diluents [6], [7] and [27]. The improvement of buck semen cryopreservation technologies requires in-depth knowledge of the properties of current extenders [29].

A 20 μl aliquot of this phage stock was added to 180 μl of rat blood (i.e. a 1 in 10 dilution) and 20 μl of this dilution was added to another 180 μl of rat blood. This serial dilution was continued to an expected 3 PFU/ml concentration. Plaque assays were carried out in triplicate and the average PFU/ml ± S.D. was plotted via the concentration calculated from phage stock. This curve was used to correlate

the actual phage stock concentration to concentrations detected from blood samples. Linear regression analysis was used to construct the equation of the line. The correlation coefficient (R2) was also calculated to assess the linearity of the data. Where appropriate, statistical analyses of the results were performed with a one-way analysis of variance, and a two-way analysis of variance (ANOVA). In all cases p < 0.05 was taken to represent a statistically SCR7 ic50 significant difference. The software package used was GraphPad Prism 5 (GraphPad software Inc., San Diego, California, USA). The images of the PC MN arrays are presented in Fig. 3. The mean height and base diameter for the PC MNs were approximately 995 μm and 750 μm, respectively. The hollow bore diameter was ≈100 μm. The aspect ratio was 1.3. The X-ray tomography images illustrate both the MN array and also the structure of the reservoirs at the base of each MN. The He-ion technology

produced ultra sharp images of the PC needles. The rich surface specific information is due to the unique nature of the beam- sample interaction. From the selleck chemicals llc insertion forces studies of the PC arrays prior to fabrication of the MN device, it was observed that, at all Amobarbital three forces investigated (i.e. 0.05, 0.1 and 0.4 N/needle), MNs penetrated the SC of the skin. Therefore, 100% penetration efficiency was observed, regardless of the applied force.

Light microscope analysis showed that no decrease in MN height was observed upon removal from skin, regardless of the force of application. Fracture force studies carried out on the MNs can be observed in Fig. 4a. At forces of 0.05 N/needle, there was no significant change in MN height. However, when the axial force was increased, the% reduction in height increased. Fig. 4b shows the morphology of MNs following 0.4 N/needle force application, with apparent damage at the tip of the needles. The 2D OCT image of the MNs following insertion into neonatal porcine skin is illustrated in Fig. 5. It was found that the MNs penetrated to an approximate depth of 700 μm and created a pore of approximate width 600 μm whilst the MNs were in situ. Fig. 5 also shows a 3D image of MNs in situ following insertion into neonatal porcine skin. It was found that, immediately following the removal of MNs from the neonatal porcine skin, the residual skin pore had a depth of approximately 210 μm, and a width of approximately 600 μm but quickly closed over (1 h, data not shown).

4). EPEC samples (E2348/69) pre-treated for 3 h with dilutions of serum or fecal extracts obtained from mice immunized with BCG-bfpA, BCG-intimin, Smeg-bfpA or Smeg-intimin, were added to HEp-2 monolayers cultivated on coverslips. As a negative control, EPEC (E2348/69) samples were similarly pre-treated with dilutions of serum

or feces collected prior to the immunizations. After incubation for I-BET-762 cost 3 h at 37 °C, the coverslips were stained and examined by light microscopy. Untreated EPEC (E2348/69) typically displays a localized pattern of adhesion, generating tight microcolonies of bacteria on the epithelial cell surface. As shown in Fig. 5A–C, adherence of EPEC (E2348/69) cells pre-treated with dilutions of immune serum or fecal extracts was blocked by over 90%. In contrast, in EPEC (E2348/69) cells pre-treated with dilutions of serum or feces collected before immunization, adherence was blocked by less than 5%. Attenuated M. bovis BCG vaccine strains have been intensively investigated as a vehicle for delivering heterologous antigens and allowing the induction of both humoral (mucosal and systemic) and cell-mediated immune responses [21]. In this study, we used recombinant BCG that expressed BfpA or intimin Crizotinib cell line as vaccines against EPEC. As an alternative,

M. smegmatis was also used to present the BfpA and intimin antigens to the host. It is interesting to note that the recombinant strains of both species were able to induce systemic and mucosal BfpA and intimin-specific antibody responses with adherence-neutralizing activity following oral administration to mice. This evidence demonstrates that the different rBCG-EPEC or Smeg-EPEC vaccine strains are potential live vectors for the generation

ID-8 of strategies to prevent EPEC. Three important qualities for a recombinant vaccine were positively evaluated in our study. First, a live attenuated vaccine was constructed with the ability to express two important proteins, BfpA and intimin, involved in the pathogenesis of EPEC. Second, the expression of the recombinant proteins induced specific and long lasting immune response in immunized mice, characterized by serum and mucosal IgG and IgA antibodies. The third important property of our recombinants is that the induced antibodies were able to prevent, in in vitro EPEC adherence to HEp-2 cells. IgA production was probably enhanced by the adjuvant effects of mesoporous silica SBA-15 [20]. SBA-15 is a nontoxic positive modulator of the mucosal immune response even in low immune responsive mice and is a natural candidate to be included as an adjuvant in an anti-EPEC vaccine. The anti-EPEC antibodies specifically recognize recombinant and native BfpA and intimin proteins free in solution and naturally fixed on the bacterial cell surfaces (Fig. 1A and B). The significant production of TNF-α and IFN-γ identifies BfpA and intimin as inducers of cellular immunity [22] and [23].