Detailed search strategies are described in Appendix 1 on the eAddenda. Citation tracking was performed by manually screening click here reference lists of reviews and relevant papers about constructs of therapeutic alliance. Papers were not excluded on the basis of the language of publication. Two reviewers (RZP and VCO) screened all relevant titles and abstracts and selected 69 potentially relevant papers. Both reviewers independently evaluated the full reports for eligibility. Disagreements were resolved by discussion. Studies were included if they met specific eligibility criteria regarding inhibitors settings, participants, therapeutic alliance constructs, coding procedures, and communication

factors. Study design: To be included, studies had to investigate the association between communication factors (interaction styles, verbal

factors, or non-verbal factors) and constructs of the therapeutic alliance (collaboration, affective bond, agreement, trust, or empathy), measured during encounters between health practitioners and patients. Settings: To be included, studies had to investigate any encounter between patients and clinicians in primary, secondary, or tertiary care settings. Participants: RG7204 research buy Studies investigating interactions between qualified clinicians and real patients were included. Studies including students as practitioners and standardised or virtual patients were excluded. However, studies including a mixed sample of real and standardised patients were eligible if data were presented separately. Interactions in highly specific clinical scenarios such as those with patients with mental illness and deaf or mute patients were excluded

as these interactions have features that may not allow generalisation to wider settings. Communication factors: There was no restriction on the type of communication factors included in this review. These factors were categorised as belonging to one of three groups: interaction style, verbal factors, or non-verbal factors. Interaction style was defined as a communication factor that exhibits aspects of both verbal and non-verbal factors simultaneously. Therefore, interaction style could incorporate features such as affective connection (friendly or personable distance), 3-mercaptopyruvate sulfurtransferase orientation (problem-focused or patient-focused), scope of information (biomedical and psychosocial), openness to patient, sharing of control, and negotiation of options ( Flocke et al 2002). Verbal factors include greetings, facilitation, checking, open-ended, and encouraging questions. Non-verbal factors include posture, facial expression, and body orientation. Therapeutic alliance constructs: To be included studies had to have assessed any construct of therapeutic alliance (for example, collaboration, affective bond, agreement, trust, or empathy). There are several ways to assess communication factors.

In this study, which included predominantly white adults aged ≥65 years who were

naïve to PPV, the immunogenicity and safety responses to the three viral subtypes in TIV (A/H1N1, A/H3N2, and B) and each selleck screening library of the 13 serotypes (serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, and 23F) in PCV13 after concomitant administration of PCV13 and TIV were directly compared with TIV (and placebo) or PCV13 administered after TIV. A clinically meaningful, empirically determined level of antibodies against pneumococcal or influenza antigens that is protective against disease in adults is lacking. A correlation between antibody levels and protection against invasive pneumococcal disease was demonstrated previously in CT99021 clinical trial children [18]. Therefore, as in most vaccine trials, the endpoints of the present trial were based on a comparison of the relative changes in immune response between administration of the vaccines separately or together [19], [20] and [21].

For TIV antigens, the immune response correlates of protection are inhibitors considered to be acceptable levels of serum antibody to the individual vaccine hemagglutinins as measured by HAI and described in “Note for Guidance on Harmonisation of Requirements for Influenza Vaccines” [16]. The analysis of TIV (A/H1N1, A/H3N2, and B) immune responses, based on the proportion of responders achieving at least a 4-fold rise in HAI titre, showed that noninferiority of PCV13 + TIV relative to TIV was met for A/H1N1 and B; for A/H3N2, the difference in proportions of responders was −4.6%, with a lower limit of the 95% CI of −10.4%, which was slightly lower than the more than −10.0% predefined margin of noninferiority. However, it was noted that in contrast

with the other two virus subtypes, the mean predose-1 titres for A/H3N2 were quite high, perhaps reflecting crotamiton pressure from A/H3N2 epidemics that occurred in the years prior to the study. In the regions where the study was conducted, H3N2 predominated over H1N1 and B in the 2006–2007 season [22]. Higher pre-immunization titres may limit the likelihood of demonstrating 4-fold responses, and the lower frequency of response would be expected to impact the ability to demonstrate noninferiority. Notably, H3N2 responder rates at an HAI titre ≥40 were comparable in the PCV13 + TIV and Placebo + TIV groups, indicating a high likelihood of protection against H3N2. In fact, all criteria proposed in the EMA “Note for Guidance on Harmonisation of Requirements for Influenza Vaccines” [16] were exceeded for all three TIV antigens (H1N1, H3N2, and B) when TIV was administered with PCV13. The data support the conclusion that TIV is sufficiently immunogenic when given concomitantly with PCV13, and that protection against influenza is likely to be clinically indistinguishable from that provided by TIV alone.

These properties are very promising devices for gene therapy of new age (Cytoplasmic Gene Therapy) because of its genotoxicity-free nature. Further, it is non-pathogenic for humans. Since Sendai virus is a murine parainfluenza virus (PIV) with certain homologies to human PIV, it was tested

as xenotropic vaccine in African Green monkeys and humans without any significant adverse reactions [34] and [35]. Recombinant SeV vector carrying human PIV was also tested in rats [36] and [37]. Further, recombinant SeV vaccine for human immunodeficiency virus (HIV) infection is going to be tested in humans (http://www.dnavec.co.jp/en/index.html). Thus, safety of Sendai virus vector is gradually established. We inserted mouse IL-10 cDNA to construct rSeV-Aβ with the aim of helping Modulators antibodies productions and suppressing Th1 type T cell activations. Nasal administration of rSeV-Aβ without IL-10 had less effect to remove BIBW2992 Aβ depositions (data not shown). Recently, soluble Aβ oligomers, but not fibrils nor selleck compound monomers, have been considered responsible for cognitive dysfunction prior to the formation of Aβ plaques [22], and Aβ*56, a 56-kDa soluble Aβ dodecamer was found responsible in Tg2576 mice [29]. Our nasal vaccine efficiently reduced not only senile plaque amyloid but also the contents of Aβ*56 oligomer without changing sAPPα and improved cognitive dysfunction in water

maze, Y-maze and contextual fear test which could evaluate hippocampus-related cognition. Thus, our vaccine, if applicable, can be given at the stage of mild cognitive impairment or earlier. Aβ is released from presynaptic sites and deposited in Dichloromethane dehalogenase extracellular plaques [38], and APP and synaptophysin are co-localized at the growth cones of developing neurons in culture [39]. These reports have indicated that Aβ deposition plays an important role in degeneration of presynaptic structures. In addition, it is reported that Aβ oligomers

directly disrupt synaptic structures [40]. In our study, synaptophysin staining showed amelioration of presynaptic degeneration following our nasal vaccine at 24 months old, suggesting prevention of synaptic degeneration or repair of synaptic structures after removal of Aβ deposits including Aβ oligomers. Our next plan is to see whether Tg2576 mice show improvement of cognitive functions by eliminating senile plaque amyloid even at 24 months old. In conclusion, a new vaccine using Sendai virus vector with Aβ and IL-10 cDNA was developed. A nasal administration of this vaccine reduced amyloid burden including Aβ oligomers significantly in AD mice and improved cognitive functions without causing side effects such as brain inflammation. This vaccine can be used to treat and prevent Alzheimer disease. Authors are grateful to Dr. Y. Noda at Meijo University, Dr. T. Nagai at Nagoya University, and Dr. M.

Estimates of infected hepatocyte numbers responsible for subsequent blood-stage parasite load and growth in vaccinees proved to be a good predictor of time to slide positive parasitaemia across all challenged subjects. This study was designed to assess a possible liver stage effect of vaccination, AZD6244 chemical structure but if a significant blood stage effect had been anticipated then a blood stage challenge

protocol [29] may have been preferable. There is an increasing consensus in the malaria vaccine development field that multiple antigens will be required in a vaccine to achieve high levels of efficacy in field trials. Heterologous prime-boost immunisation has been one of the very few approaches to successfully induce sterile efficacy in any human vaccinees and this study has assessed a polyprotein

approach to broadening the immunogenicity of the induced T cell responses. Our results suggest that there may be limits to the insert size that will be readily immunogenic in humans, at least using standard vaccinia promoters. Hence other vector design strategies, such as the use of multiple promoters and insertion sites [30], or mixtures of single vaccines may be more suitable for exploiting the great capacity of poxviruses to express foreign antigens. This study was principally funded by the European Malaria Vaccine Initiative (EMVI) now European Vaccine Initiative (EVI). The authors would PD0325901 order like to thank Odile Leroy and Egeruan Imoukhuede for advice and support. Additional inhibitors support from the Wellcome Trust and the NIHR Oxford Biomedical Research Centre is gratefully acknowledged. SG is a Jenner Institute Investigator ADAMTS5 and AVSH is a Wellcome Trust Principal Research Fellow. “
“Complex

antigenic polymorphisms present a significant challenge for design of a vaccine against the malaria parasite Plasmodium falciparum. Although partial protection offered by the current leading malaria vaccine candidate RTS,S appears not to be compromised by limited polymorphism in the pre-erythrocytic circumsporozoite protein [1], the problem of polymorphism is likely to be more important for vaccines based on blood-stage parasite proteins that are targets of naturally acquired immunity [2] and [3]. The extracellular merozoite that invades erythrocytes is an important target of immunity [4], and a leading vaccine candidate is the most abundant surface component, merozoite surface protein 1 (MSP1) which is expressed as a large ∼200 kDa precursor that needs to be proteolytically processed to allow merozoite maturation [5]. Antibodies to several parts of the protein can inhibit this processing [6], but most research has focused on the C-terminal region, particularly the 19 kDa C-terminal fragment MSP1-19 [7], [8], [9] and [10].

3C). When analyzing the expression of CD137 in CD4+ T cells, mice vaccinated

with 10 μg mice showed a reduced expression, which diminished even more after these cells were re-stimulated in vitro with 10 μg LPG ( Fig. 3D). Together these data show that L. mexicana LPG negatively regulates CD8+ cell activation by enhancing PD-1 expression and concomitantly reducing CD137 expressions, where the degree of the modulation depends upon the dose of LPG used for immunization as well as the dose of the subsequent stimulus. In contrast to CD8+ T cells, vaccination with find more LPG had no inhibitory effect on CD4+ T cells, since it did not modify their PD-1 expression and re-stimulation with LPG reduced their PD-1 expression. Thus, LPG vaccination selleck chemical seems to exert the inhibitory effect only on CD8+ T cells, in a dose dependent fashion. To analyze whether parasite infection modulates PD-1 expression

in T lymphocytes, BALB/c mice were infected in the earlobe dermis with 1 × 104 or 1 × 105L. mexicana promastigotes. Mice were sacrificed prior to ulceration of the lesions. Splenocytes were isolated and re-stimulated in vitro with 1, 5 or 10 μg LPG during 24 h and PD-1 as well as CD137 were analyzed. We found that PD-1 expression is enhanced in CD8+ T cells of mice infected with 1 × 104 (0.5-fold) or 1 × 105 (3.6-fold) parasites, as compared to CD8+ T cells from non-infected mice ( Fig. 4A). In vitro stimulation with all three doses of LPG showed the same high expression of PD-1. The analysis of CD137 in CD8 T cells showed a 40% down-regulation in mice infected with 1 × 104 promastigotes, whereas mice infected with 1 × 105 promastigotes showed a similar expression as non-infected mice. In vitro re-stimulation with LPG did not alter CD137 expression ( Fig. 4B). CD4+ lymphocytes showed a minimal increase in PD-1 expression after infections with either number L. mexicana parasites, and showed no changes despite secondary stimuli with LPG ( Fig. 4C). Furthermore, Casein kinase 1 the expression of CD137 in CD4+ T

cells of infected mice also remained unaltered. The only up-regulation of this activation marker was observed in CD4+ T cells of mice infected with 1 × 105 Libraries parasites after they were re-stimulated in vitro with 5 μg LPG ( Fig. 4D). In conclusion these results show that L. mexicana infection induces significantly enhanced PD-1 expression only in CD8+ T cells, in a dose-dependent fashion. The reduced expression of CD137 in association with the increased levels of PD-1 in these CD8+ T cells seems to indicate that they resemble an exhausted phenotype. PD-1 is minimally expressed in CD4+ cells during L. mexicana infections and not altered by in vitro LPG stimuli, showing that L. mexicana exerts a stronger inhibitory effect on CD8+ T cells, as compared to CD4+ T cells.

Biochemical parameters like Serum Glutamic Oxaloacetic Transaminase (SGOT) and Serum Glutamic Pyruvic Transaminase (SGPT), Serum Alkaline Phosphatase (ALP), Serum Total bilirubin (T. Bil) were estimated by using commercial reagent kits in autoanalyzer (RM4000, Biochemical systems International, Italy). 15, 16, 17 and 18 Acute toxicity studies in mice

revealed that the extracts up to 2000 mg/kg produced no sign of SRT1720 toxicity or mortality. Qualitative phytochemical screening for different extracts of G. gynandra revealed the presence of steroids, terpenoids, glycosides, tannins, alkaloids, flavonoids, phenols and carbohydrates ( Table 1). The phenolic content of various extracts of G. gynandra were ranging from 13.21 ± 0.66 to 72.80 ± 0.22 (mg/g). The hydroalcoholic extract has more phenolic content (72.80 ± 0.22 mg/g) than other extracts. The alkaloidal content of extracts was ranging from 8.91 ± 0.10 to 16.68 ± 0.21 (mg/g). Antiinfection Compound Library The methanolic extract has more alkaloidal content (16.68 ± 0.21 mg/g) than other extracts ( Table 2). The different extracts of G. gynandra were found to possess concentration dependent free radical scavenging inhibitors activity on tested free radicals ( Table 3). The mean IC50 values for superoxide radical scavenging activity of hydroalcoholic, methanolic, ethyl acetate and hexane extracts G. gynandra were found to be 150.5 ± 1.5 μg,

126.5 ± 1.3 μg, 259.2 ± 2.1 μg and 575.0 ± 2.3 μg. The mean IC50 values for hydroxyl radical scavenging activity of hydroalcoholic, methanolic, ethyl acetate and hexane extracts of G. gynandra were found to be 226.5 ± 2.1, 164.3 ± 1.8, 452.0 ± 2.5 and 709.5 ± 3.2 μg. The mean IC50 values for DPPH radical scavenging activity of hydroalcoholic, methanolic, ethyl acetate and hexane extracts of G. gynandra were found to be 108.25 ± 2.3,

87.9 ± 1.1, 239.4 ± 2.3 and 340.0 ± 2.2 μg. The order of activity as follows: ascorbic acid > methanolic extract > hydroalcoholic extract > ethyl acetate extract > Dipeptidyl peptidase hexane extract. The CCl4-induced hepatotoxicity model is widely used to evaluate the hepatoprotective activity of drugs and plant extracts. The hepatoprotective effect of different extracts of G. gynandra at dose of 100, 200 and 400 mg/kg assessed (percentage protection) by measuring liver related biochemical parameters (SGOT, SGPT, ALP and total serum bilirubin) following CCl4-induced hepatotoxicity. In our studies, CCl4-damaged rats that were previously treated with extracts showed a significant decrease in serum GOT, GPT, ALP and T. bilirubin. This is evidence that both stabilization of the plasma membrane and repair of CCl4-induced hepatic tissue damage. The standard drug silymarin and higher dosages of extracts showed a strong hepatoprotective effect against CCl4-induced liver injury. Group I showed no significant change in the biomarkers of enzymes (SGOT, SGPT, ALP and total serum bilirubin) levels.

Recording brain activity during the task with functional magnetic resonance imaging (fMRI) allowed us to compare observed choices, decision latencies, and brain activity to those predicted by three computational models that embodied different hypotheses about how humans learn about and choose between categories. The first model learned the mean and variance of the categories in an optimal Bayesian framework (Bayesian model), the second model learned the value of action in a given

state, i.e., angle (Q-learning [QL] model), and the third model simply maintained the most recent category information in memory (working memory [WM] model). These models allow us to compare the hypotheses that category judgments in an unpredictable environment are driven by strategies that rely on “model-based” optimal estimation buy Apoptosis Compound Library of uncertainty (Bayesian), “model-free” habit learning (Q-learning), or a cognitive strategy based on short-term maintenance (working memory). We report a number of new findings. First, both the Bayesian and the WM models encoded unique variance in choice, reaction time (RT), and brain activity, suggesting that participants use a mixture of model-based categorization strategies. Second, participants’ tendency to use a decision policy Selleckchem PLX4032 that incorporated category

variance depended aminophylline on the volatility of the environment, with the Bayesian model approximating human performance more closely in relatively unchanging environments, and neural signatures of choice and learning modulated by category variability only during stable periods; by contrast, the WM model prevailed when the environment was more volatile. Finally, different strategies

were associated with dissociable patterns of decision-related brain activity, with fMRI signals predicted by the Bayesian model observed in the striatum and medial prefrontal cortex (PFC), but brain activity predicted by the working memory strategy activating visual regions, and the dorsal frontal and parietal cortex. Together, these results suggest that participants use cognitive strategies involving the short-term maintenance of information when making decisions in volatile environments but gradually come to rely on information about category uncertainty to make more optimal choices as learning progresses. On each of 600 trials, 20 participants viewed an oriented stimulus (full-contrast Gabor patch) that was drawn from one of two categories defined by orientation, with angular means on trial i   of μˆia and μˆib and variances σˆia and σˆib ( Figure 1A). Subjects received no instructions regarding the categories but were required to learn about them by trial and error via an auditory feedback tone following each decision epoch of 1500 ms.

, 2005; Lau and Glimcher, 2008; Cai et al., 2011; Kim et al., 2009, 2013). In addition, signals see more necessary for updating the value functions, including the value of the chosen action and reward prediction errors, are also found in the striatum (Kim et al., 2009; Oyama et al., 2010; Asaad and Eskandar, 2011). Moreover, the dorsolateral striatum, or the putamen, might be particularly involved in

controlling habitual motor actions (Hikosaka et al., 1999; Tricomi et al., 2009). Although the striatum is most commonly associated with model-free reinforcement learning, additional brain areas are likely to be involved in the process of updating action value functions, depending on the specific type of value functions in question. Indeed, signals related to value functions and reward prediction errors are found in many different areas (Lee et al., 2012). Similarly, using a JQ1 cell line multivariate decoding analysis, signals related to rewarding and punishing outcomes can be decoded from the majority of cortical and subcortical areas (Figure 2; Vickery et al., 2011). The neural substrates for model-based reinforcement learning are much less well understood compared to those for Pavlovian conditioning and habit learning (Doll et al., 2012). This is not surprising, since the nature of computations for simulating the possible outcomes and their neural implementations might vary widely across various decision-making problems. For

example, separate regions of the frontal cortex and striatum in the rodent brain might underlie model-based reinforcement learning (place learning) and habit learning (response learning; Tolman et al., 1946). In particular, lesions in the dorsolateral striatum and infralimbic cortex impair habit learning, while lesions in the dorsomedial striatum

and prelimbic cortex impair model-based reinforcement learning (Balleine Dichloromethane dehalogenase and Dickinson, 1998; Killcross and Coutureau, 2003; Yin and Knowlton, 2006). In addition, lesions or inactivation of the hippocampus suppresses the strategies based on model-based reinforcement learning (Packard et al., 1989; Packard and McGaugh, 1996). To update the value functions in model-based reinforcement learning, the new information from the decision maker’s environment needs to be combined with the previous knowledge appropriately. Encoding and updating the information about the decision maker’s environment might rely on the prefrontal cortex and posterior parietal cortex (Pan et al., 2008; Gläscher et al., 2010; Jones et al., 2012). In addition, persistent activity often observed in these cortical areas is likely to reflect the computations related to reinforcement learning and decision making in addition to working memory (Kim et al., 2008; Curtis and Lee, 2010). Given that persistent activity in the prefrontal cortex is strongly influenced by dopamine and norepinephrine (Arnsten et al., 2012), prefrontal functions related to model-based reinforcement learning might be regulated by these neuromodulators.

Genetic mutations in mice that disrupt barrel development typically disrupt only the columnar distribution of neurons in L4 and leave the clustering of thalamocortical axons intact (Li and Crair, 2011). A handful of the most severe barrel map mutants, including barrelless mice and GAP-43 KO mice, have no hint of either thalamocortical axon clustering into barrels or L4 cytoarchitecture resembling barrel walls. Previous experiments that disrupted neuronal activity or cortical

glutamatergic signaling pharmacologically or genetically had mixed effects on barrel development ( Li and Crair, 2011). For instance, interfering with cortical glutamatergic receptors www.selleckchem.com/products/Methazolastone.html ( Schlaggar et al., 1993, Iwasato et al., 2000 and Wijetunge et al., 2008) disrupts cortical barrel cytoarchitecture, but has no effect on thalamocortical axon clustering into a barrel pattern. Similarly, interfering with neuronal activity pharmacologically

( Chiaia et al., 1992) or disrupting thalamocortical neurotransmission genetically ( Lu et al., 2006 and Narboux-Nême et al., 2012) interferes with the emergence of cortical barrel cytoarchitecture but has no effect on Ruxolitinib price thalamocortical axon clustering. Notably however, the interventions used in these studies did not completely block thalamocortical glutamatergic neurotransmission, but rather interfered with restricted subsets of glutamate receptors or decreased the probability of neurotransmitter release without eliminating thalamocortical neurotransmission or changing synaptic strength. A likely consequence of the incomplete nature of these manipulations is that barrel cytoarchitecture

is disrupted, Cell press but thalamocortical axon clustering and cortical laminar cytoarchitecture are preserved. In contrast to these previous studies, the manipulation we reported here nearly completely blocks thalamocortical neurotransmission (ThMunc18KO mice) or nearly completely prevents thalamocortical neurons from releasing glutamate (ThVGdKO mice). We suggest that the more comprehensive disruption of thalamocortical glutamatergic neurotransmission we achieved produced the correspondingly more dramatic effects on cortical barrel, laminar, and neuronal cytoarchitectural development. We observed that Vglut1 was capable of compensating for the absence of Vglut2 in thalamocortical neurons in vivo. The same is not true in cultured neurons, where thalamic cells that lack only Vglut2 have dramatically disrupted neurotransmitter release ( Moechars et al., 2006). Neurons in the ventrobasal thalamus are known to express both Vglut1 and Vglut2 in a dynamic fashion through the course of development ( Barroso-Chinea et al., 2008 and Nakamura et al., 2005), as do single axon terminals in L4 of barrel cortex during the first week after birth ( Nakamura et al., 2005). The observed difference in compensation by Vglut1 for Vglut2 may reflect a difference in the dynamic regulation of these two Vglut gene family members in vivo and in vitro.

DNA transformation procedure was performed using QIAGEN EZ competent cells and 2 μl of ligation-reaction per the manufacturer’s instructions. Competent cells containing the vector with PCR product

insert were detected with ZD1839 mouse blue/white screening by plating 50 μl of the transformation mixture on Luria-Bertani (LB) broth agar plates supplemented with 100 mg/ml carbenicillin, 100 mM of Isopropyl β-d-1-thiogalactopyranoside, and 40 mg/ml of β-Gal reagent. Two to three colonies, if available, were isolated and propagated in LB broth supplemented with 100 mg/ml carbenicillin. Plasmid DNA was isolated using Mini-prep kit (QIAGEN) per the manufacturer’s instructions. Bi-directional sequencing of the inserts from the clones (2–3 per isolate) was performed using M13 F

and M13 R plasmid specific primers at the Integrated Biotechnology Laboratories (The University of Georgia, Athens, GA 30602). The sequences obtained were compared to those in GenBank. Sequences were also aligned with other related sequences using the multisequence alignment ClustalX program and the chromatograms were manually examined to detect polymorphisms (Thompson et al., 1994). Phylogenetic analyses were conducted using MEGA (Molecular Evolutionary Genetics Analysis) version 4.0 program (Kumar et al., 1993). The neighbor-joining and minimum check details evolution algorithms use the Kimura 2-parameter model and maximum parsimony uses a heuristic search. The GenBank accession numbers of sequences obtained in this study are listed in Table 1. The two green-winged saltators were found dead while housed in the CETAS-IBAMA and clinical signs were not recorded. All others birds demonstrated difficulty eating and drinking and at physical examination there were yellow and friable plaques on the tongue and oral mucosa consistent with trichomonosis. The immature striped owl was lethargic, emaciated, had ruffled Histone demethylase feathers,

salivated excessively, had difficultly closing its mouth due to abundant caseous material, and exhibited open mouth and loud breathing. The immature American kestrel had multifocal yellow plaques on the oral mucosa when presented to the veterinarian and during hospitalization the plaques increased in size and became diffuse on the oral mucosa and tongue. Four days later the kestrel demonstrated severe dyspnea and died the following day. The toco toucan was lethargic and had difficulty standing. Necropsy revealed that all birds were thin and dehydrated. Multifocal yellow, friable plaques were observed on the surface of the tongue in the owls, toucan and American Kestrel. Friable and yellow plaques and/or nodules also were observed on the oral mucosa, upper mouth, pharynx and larynx of the American kestrel (Fig. 1).