(2008), showing common reactivity to spots identified as GroEL and SodB. Both spots are reported (McCool et al., 2008) to be good markers of CSD. However, our results have not

completely confirmed their results: firstly, we found a lower rate of CSD patients’ sera reactivity to SodB [sensitivity (Se) 28.5%] compared with that reported by McCool et al. (2008) (71%) and sera from IE patients (Se 86%), and secondly, a huge rate of cross-reactivity to GroEL among BD was found [specificity (Sp) 25%] in contrast to that obtained by McCool et al. (2008), and GroEL was highly specific (100%) (Table 2). This result is not surprising considering that GroEL is a very well-conserved protein. On comparing our results with those of Eberhardt et al. (2009), who tested 33 sera IFA≥200 with active check details Bartonella infection, it was found that there was common reactivity STA-9090 nmr to well-conserved antigens, such as GroEL, groES, EF-Ts, EF-Tu, Pnp and SodB, but they obtained a very heterogeneous pattern of reactivity compared with our results (McCool et al., 2008). The best hits were dihydrolipoamide succinyltransferase (SucB), EF-Tu and Omp (BH11510) that has also been identified as the best marker of IE due to Bartonella in our study. In this study, the reactivity to this protein was not detected in the sera from patients with CSD; therefore, it is difficult to compare the serological parameters with those obtained by Eberhardt et al. (2009), because they have

treated all patients together, without establishing a distinction between CSD and IE. However, on combining (IE+CSD) together, the Se and Sp obtained for Omp (BH 11510) are very similar to those obtained by Eberhardt et al. (2009) (Table 2). We also obtained a cross-link with two other proteins: pnp and SodB. For the first one, we obtained a value of Se for patients with CSD that was very similar

to their results (Eberhardt et al., 2009). However, in our case, pnp exhibited a high level of cross-reaction, which is in not contradiction with the German results (Eberhardt et al., 2009). Similarly, for CSD, we obtained a value of Se that was in the same range as that obtained by Eberhardt et al. (2009) for CSD patients, but the Sp was higher in our study. Although consistent reactivity to a single spot for all serum samples was not observed, 13 candidate proteins were detected for IE and CSD sera (Table S1). The best candidate clinical biomarkers for IE sera that did not react with CSD sera were HbpD, Pap31 and BH11510 (OMP) (sensitivity ≥57%) (Table 2). Among the BD, the cross-reactivity to B. henselae proteins was not frequently seen when compared with serum samples from CSD patients. Some isoforms were commonly found to be immunoreactive with sera from CSD patients, including ATPD, DnaK, FusA, GroEL and Pnp (Figs 2–4), while the immunoreactivity of GroEL was also seen in serum samples from BD. PCA analysis showed some similarities in the immunoreactivity pattern between CSD and BD (Figs 1, 3 and 4).

(The ISTM Certificate in Travel Health® calls for familiarization with pediatric aspects by including many BAY 73-4506 clinical trial questions on the subject.) What is presently lacking is a uniform definition of “children,” a dilemma which extends into the travel medicine literature. In recent articles in the JTM and elsewhere, authors of major articles use 14, 16, 18, and 20 years of age as the upper age limit of their subjects. And while the authors do segregate their subjects into groups by age (apparently agreeing that infants have little in common with older teenagers),

there is no uniformity in the segregations, making comparisons difficult. Moreover, some authors compare travel-related illness among adults versus those in children, using selleckchem the author’s definition of “children.” (The American Academy of Pediatrics defines pediatrics as “beginning with the fetus and continuing until the age of 21 years—and longer if it is an ongoing problem that is basically a childhood condition.”)8 The many recent studies in this issue and elsewhere on children returning home ill should not give a false impression that taking children overseas is particularly hazardous. Until recently, little data existed on the specific morbidity and mortality though anecdotal experience and informal surveys suggested that serious illness and deaths were

rare.9 The present studies reinforce those impressions. These studies limit themselves to describing the types of illnesses seen in returning children and the vast majority of the illnesses were relatively minor. This was true even for children who go on adventurous trips and for very young children. But the studies included only children seen in specific large Protein tyrosine phosphatase medical centers with which the authors are affiliated. Excluded are children who returned home ill but were seen at other medical centers, by private physicians, or not at all. But likely, children with serious travel-related illnesses

would have gravitated to the larger medical centers. No deaths were reported. But deaths occurring overseas could have escaped inclusion in the studies. Experienced travel medicine practitioners, even those who possess little formal training in caring for children, generally possess the expertise to counsel parents on keeping their children healthy when they travel. And generally such practitioners should be the first consulted when children return home ill. The articles on pediatric travel medicine in this issue of JTM add substance to the growing literature on the subject, are evidence based, and all the articles reach the same general conclusion, that the risk of major travel-related illnesses in children is quite small. The author states he has no conflicts of interest to declare. “
“Background.

14 Subjective data revealed that, despite apprehension, social media-naïve health care professionals quickly learned how to use social media to deliver a health care message. However, of the health care professionals who decided to use Twitter only around 20% continue to use it as a professional resource beyond the confines of the module. One limitation of this study was the application of metrics that determine the ‘impact’ of online activity. Besides the metrics that we collected there is little else to assess one’s online

impact. The website, Klout, has been established to endeavour to do this and has been proposed as a useful way of assessing online impact in medicine.15 We did not use Klout, as it requires the individual’s Selumetinib Selleckchem KU57788 registration across the social media channels nor is it able to assess the quality of material being posted. With the latter in mind and with no previous experience of tweeting or creating video content, some of the content could have been improved

with closer attention to production values; nonetheless, the attempts demonstrated the subjects’ ability to communicate useful and accurate information about diabetes. Similarly, it is encouraging that some students have continued to use these media

channels beyond the course requirements, gaining skills and experience in disseminating their clinical knowledge to a wider audience. In addition, we recognise that it is difficult to draw firm conclusions regarding the views of subjects participating in this study when only a minority answered the questionnaire. Although creating a potential bias, the observations are Astemizole still of interest and do support the observation of a minority trend regarding the long-term use of Twitter. With the rising use of social and mobile media in health care, the opportunities for promoting health, improving care and communicating with peers should not be overlooked. Our study reveals that, despite initial apprehension, social media-naïve health care professionals were successful in conveying a professional message through Twitter and YouTube. Furthermore, social media use continues in a substantial number of subjects beyond the confines of the study, suggesting appreciation for how social media may be used in inter-health professional communication as well as the care of the patient with chronic disease. There are no conflicts of interest declared. References are available in Practical Diabetes online at www.practicaldiabetes.com.

The proportions of patients with hypertension, type 2 diabetes mellitus and current or past smoking history were 38.2, 12.7 and 28.5%, respectively. A total of 6136 patients (31.6%) were coinfected with HIV and HCV (HIV/HCV). Table 1 summarizes the characteristics of our patients with HIV infection only and with HIV/HCV coinfection. In univariate analysis, HCV coinfection was associated with a significantly reduced prevalence of hypercholesterolaemia (18.0% in

HIV/HCV vs. 30.7% in HIV-only patients; P<0.001) and hypertriglyceridaemia (49.6%vs. 55.7%; P<0.001). Coinfected patients were also less likely to meet the composite endpoint of laboratory-defined dyslipidaemia or being on lipid-lowering therapy (55.6%vs. 65.4%; selleck chemical P<0.001). HCV-coinfected patients were significantly more likely than HIV-monoinfected patients to have a diagnosis of hypertension (43.8%vs. 35.6%, respectively; P<0.0001) or type 2 diabetes mellitus (16.2%vs. 11.1%; P<0.0001) or to have a past or current smoking history (36.7%vs. 24.7%; P<0.0001). The proportions of HIV-monoinfected and HIV/HCV-coinfected patients with antiretroviral learn more exposure were virtually identical (80.0 and 79.9%, respectively). The mean duration of ART exposure was slightly lower in HIV/HCV-coinfected than in HIV-monoinfected patients (1.87 years vs. 1.96 years, respectively; P=0.006). During the observation period, representing 76 376 patient-years, a total of 278 AMIs were diagnosed; 171 among HIV-monoinfected

and 107 among HIV/HCV-coinfected patients. Rates of AMI were significantly higher among HIV/HCV-coinfected patients than HIV-monoinfected patients: 4.19 vs. 3.36 events/1000 patient-years, respectively (P<0.001).

During the same period, 868 CVDs were diagnosed; 555 in HIV-monoinfected and 313 in HIV/HCV-coinfected patients. Rates of CVD were also significantly higher among HIV/HCV-coinfected patients: 12.47 vs. 11.12 events/1000 patient-years for HIV/HCV-coinfected and HIV-monoinfected patients, respectively (P<0.001). Unadjusted hazard ratios (HRs) for AMI and CVD associated with HCV coinfection (vs. HIV monoinfection) were 1.25 [95% confidence interval (CI) 0.98–1.59; P=0.075] and 1.12 (95% CI 0.98–1.29; P=0.105), respectively (Table 2). In multivariate Cox proportional hazards analysis controlling for hypertension, type 2 diabetes mellitus, age, tobacco use and duration of antiretroviral use, HCV coinfection pheromone was independently associated with CVD (adjusted HR 1.20; 95% CI 1.04–1.38; P=0.013). Its association with AMI was not statistically significant (HR 1.25; 95% CI 0.98–1.61; P=0.072). Other factors associated with AMI in the multivariate model included greater age (HR 1.79 for each 10-year increment; 95% CI 1.60–2.01; P<0.001), hypertension (HR 2.05; 95% CI 1.57–2.67; P<0.001), and longer duration of ART (HR 1.12 for each year of use; 95% CI 1.01–1.25; P=0.0411). Type 2 diabetes mellitus was associated with increased risk of AMI in unadjusted analysis (HR 1.75; 95% CI 1.32–2.

In this study, we investigated the nematicidal effects of Bacillus spp. against plant-parasitic nematodes and identified potential genes associated INCB024360 molecular weight with nematicidal activity. The bacterial strains

and plasmids used in this study are described in Table 1. Escherichia coli strain DH5α was used as the host for all plasmids. The pMarA shuttle plasmid carries the TnYLB-1 transposon, the mariner-Himar1 transposase and a Gram-positive thermosensitive replicon (Breton et al., 2006). New plasmids and strains constructed in this study are described in the text. Luria broth (LB) was used for growing E. coli, Bacillus spp. and the OKB105 mutants. Landy culture medium was used to ferment all Bacillus isolates and mutants (Landy et al., 1948). When required, Landy medium was supplemented with adenine (12 μg mL−1) and thiamine (0.8 μg mL−1), with 5-aminoimidazole-4-carboxamide riboside (AICA-riboside, an intermediate in the purine biosynthesis pathway, 4 mM), with O-diazoacetyl-l-serine (azaserine, 550 μM) or with sulfamethoxazole (250 μM), separately. Bacterial cultures were grown in 250-mL flasks with shaking (200 r.p.m.) at 37 °C for 48 h. When required, antibiotics were added at the following final concentrations: ampicillin (Ap), 100 μg mL−1; chloramphenicol (Cm), 5 μg mL−1; kanamycin (Km), 5 or 50 μg mL−1. Nematodes

used in this study are described in Supporting Information, Table S1 and maintained as described (Iwahori Loperamide et al., 1998; Wang et al., 2007, 2009). The four cultured Selumetinib nematodes were separated using the Baerman funnel technique (Gray, 1984), surface sterilized with 3% H2O2 or 1% NaClO for 5 min and then rinsed three times with sterile distilled water before use. Fermented cultures (50 mL) were centrifuged at 17000 g for 15 min at 4 °C and supernatants then collected and tested for nematicidal activity. Fifty sterilized nematodes were transferred to a 60-mm-diameter watch

crystal with 1.5 mL of the respective supernatants. The watch crystal was placed in Petri dishes and incubated at 25 °C. The method for determining nematicidal activity was based on previously described procedures (Huang et al., 2005) and nematode viability was assessed by observation under a dissecting microscope. The respective supernatants were tested in triplicate and each experiment was repeated five times. Cold resistance of the bacterial metabolites was tested by separately incubating culture filtrates at 4 and −25 °C for 5, 10, 15, 20, 25, 30, 35 or 40 days and subsequently testing for nematicidal activity as described above. Heat resistance was tested by supernatants incubating in a 100 °C water bath for 25 min or sterilizing in an autoclave at 121 °C for 20 min before testing for nematicidal activity. Assessment of nematicidal activity of the culture filtrate components was carried out in one of two ways: 1 100-mL culture filtrates were dried with a vacuum rotary evaporator at 60 °C.

The translocation of T3SS effectors into host BGB324 manufacturer cells is the most distinctive function of T3SSs. However, the secretion of T3SS effectors is thought to be a different event from translocation (Lee & Galan, 2004) because there are several examples of exceptions in which constructs of the amino-terminal signal sequence of T3SS effectors fused

with a reporter protein can be observed in the supernatant and not inside host cells (Lee & Galan, 2004). To exclude this possibility for VocC, a translocation assay using VopC fused with the catalytic domain of CyaA was performed (Sory et al., 1995). This assay determines whether a T3SS effector–CyaA fusion is injected into eukaryotic cells by measuring intracellular cAMP levels because the activity of the CyaA catalytic domain requires calmodulin within eukaryotic cells. The wild-type strain expressing the VopC–CyaA fusion induced a high level of cAMP inside Caco-2 cells, while the ∆vocC strain did not, producing levels similar to the negative control (the T3SS2-deficient strain, vcrD2) (Fig. 3).

These results indicate that VocC is necessary for not only the secretion of VopC but also its translocation into host cells. Another characteristic of T3SS chaperones is the ability to bind their cognate effector. As expected from the screening assay used to identify T3SS2-associated chaperones (Fig. 1), VocC appeared to bind VopC. In this binding experiment, purified proteins were used to observe direct binding between the chaperone and an effector. A pull-down assay was performed using purified GST–VocC (42.6 kDa) and poly-histidine-tagged VopC (VopC–HIS; 45.9 kDa). DAPT molecular weight As shown in Fig. 4, GST–VocC coprecipitated acetylcholine with VopC–HIS, while GST alone as a negative control did not. Another presumable substrate

for VocC, VopT, fused with a poly-histidine tag showed similar binding results to GST–VocC (data not shown). In previous studies, the binding of T3SS-associated chaperones and effectors and the amino-terminal secretion signal of effectors were required for efficient secretion via the T3SS (Arnold et al., 2009). Therefore, it was important to identify the chaperone-binding domain and the amino-terminal secretion signal of VopC. First, we used a series of truncated VopC mutants fused with CyaA in a pull-down assay with GST–VocC. As shown in Fig. 5a, the domain covering at least 100 amino acids from the amino terminus of VopC was responsible for binding to VocC. Additional pull-down assays using VopC21–100–CyaA showed that VocC bound to the amino-terminal 21–100 amino acids of VopC (Fig. 5b). Next, we examined whether an amino-terminal secretion signal existed in VopC. A secretion assay using V. parahaemolyticus T3SS1-deficient strains (ΔvcrD1) expressing a series of truncated VopC mutants fused with CyaA was carried out to assess the specific secretion of VopC fusions through T3SS2 (Fig. 5c).

Cultures were grown in photoheterotrophic conditions for 45 h, at which point they are ~35 h into the stationary phase of growth. These cultures were filtered using 0.45-μm PVDF syringe filters and filtrates assayed for RcGTA activity by mixing 0.1 mL of filtrate with DW5 cells in a total volume of 0.6 mL GTA buffer (Solioz et al., 1975). After incubation for 1 h, 0.9 mL of RCV broth was added and the mixtures incubated for an additional 4 h

with shaking at 200 r.p.m. The samples were plated on YPS agar, incubated in anaerobic phototrophic conditions to select for transfer of the puhA marker, and colony numbers were counted after 48 h. RcGTA activity was calculated as a ratio relative to paired wild-type RcGTA activity in three replicate experiments. Statistically significant differences in Ibrutinib mouse RcGTA activities were identified by one-way analysis of variance (anova) in R (Chambers et al., 1993). Western blots targeting the RcGTA major capsid protein (~32 kDa) were performed on the same cultures AZD6244 datasheet used for RcGTA activity assays. For each culture, 0.5 mL of culture was centrifuged at > 13 000 g for 1 min to pellet the cells, and 0.4 mL of the resulting supernatants was carefully collected into a separate tube. The cell pellets were resuspended in 0.5 mL of TE buffer. These samples, 5 μL of cells and 10 μL of supernatants, were mixed with 3× SDS–PAGE

sample buffer, boiled for 5 min at 98 °C, and run on a 10% SDS–PAGE gel. Proteins were transferred to a nitrocellulose membrane by electroblotting in transfer buffer [48 mM Tris Base, 39 mM glycine, 20% methanol (v/v)]. The presence of equivalent total protein levels within supernatant and cell sample groups was verified

by staining the blotted membrane with Ponceau-S. The membranes were rinsed and blocked with a 5% (w/v) skim milk solution in TBST [20 mM Tris, 137 mM NaCl, 0.1% Tween-20 (v/v); pH 7.5] for 1 h. The membranes were rinsed with TBST and incubated overnight at 4 °C with a primary antibody D-malate dehydrogenase (1 : 1000 dilution in TBST) specific for the RcGTA major capsid protein (Agrisera, Sweden) (Fu et al., 2010). The membranes were washed three times in TBST, for 5 min each, and incubated with peroxidase-conjugated anti-rabbit IgG (Santa Cruz Biotechnology) (1 : 5000 dilution in TBST) for 1 h at room temperature. The membranes were rinsed three times with TBST for 5 min each, and bands detected by chemiluminescence using the SuperSignal West Femto Reagent Kit (Thermo Fisher Scientific, Canada). Images were captured on an Alpha Innotech U400 camera and then inverted and adjusted for brightness and contrast with image processing software. Motility assay tubes (Krieg & Gerhardt, 1981) were made with 0.35% agar YPS, and the stabs were incubated phototrophically at 35 °C. Tubes were photographed after 2 days of growth and the images adjusted for brightness and contrast with image processing software.

Earlier intervention remains controversial and PF-02341066 ic50 widely debated; however, a large body of evidence, from both preclinical and clinical studies, demonstrates that therapies such as dopamine neuron grafting are not, and may never be effective in subjects with severe dopamine depletion (Winkler et al., 2005; Breysse et al., 2007; Linazasoro, 2009; Truong & Wolters, 2009). Intervention, such as preserving dendritic spine morphology, together with dopamine terminal replacement earlier in disease offers therapeutic promise that does not seem probable

in advanced PD. The authors would like to thank Dr Ariel Deutch of Vanderbilt University for his valuable guidance on nimodipine pellet formation and use. We would also like to thank Dr Timothy Schallert of University of Texas at Austin for his expert guidance on behavioral test paradigms. Further, we would like to acknowledge the outstanding technical assistance of Jennifer Stancati and Brian Daley. This work is supported Selleck LY2109761 in

part by R01NS045132, P50NS058830, The Udall Center of Excellence at the University of Cincinnati, and the Michael J. Fox Foundation. Abbreviations 6-OHDA 6-hydroxydopamine CE coefficient of error GID graft-induced dyskinesia MSN medium spiny neuron PD Parkinson’s disease TH tyrosine hydroxylase TPD tapping dyskinesia “
“Communication by analogue signals is relatively common in arthropod local networks. In the locust, non-spiking local interneurons play a key role in controlling sets of motor neurons in the generation of local reflex movements of the limbs.

Here, our aim was two-fold. Our first aim was to determine the coding properties of a subpopulation of these interneurons by using system identification approaches. To this end, the femoro-tibial chordotonal organ, which monitors the movements of the tibia about the femur, was stimulated with Gaussian white mafosfamide noise and with more natural stimuli corresponding to the movements of the tibia during walking. The results showed that the sample of interneurons analysed displayed a wide, and overlapping, range of response characteristics. The second aim was to develop and test improved data analysis methods for describing neuronal function that are more robust and allow statistical analysis, a need emphasized by the high levels of background neuronal activity usually observed. We found that nonlinear models provided an improved fit in describing the response properties of interneurons that were then classified with statistical clustering methods. We identified four distinct categories of interneuron response that can be further divided into nine groups, with most interneurons being excited during extension movements of the leg, reflecting the outputs of upstream spiking local interneurons.

These are clues that tell us shame is present and, unless it is actively addressed, self-management is unlikely to deliver the healthy outcomes that the person with diabetes desires. This article addresses what shame is, its purpose, how it develops, our response to it and how

it may best be dealt with. The language of psychotherapy is unlikely to be familiar to most diabetes health carers; I have therefore employed everyday language to present Humanistic psychotherapy shame concepts in as clear a way as possible. The manner in which people with diabetes tackle, minute by minute, hour by hour and day in day out, their self-management is frequently shaped not only by their sense of personal shame but by how their diabetes carer’s own shame issues affect their consultation skills. Shame plays a major role in the eventual consequences of diabetes self-management. Copyright © Palbociclib 2014 John Wiley & Sons. “
“People with diabetes are more likely to be admitted to hospital and have longer stays in hospital than people without diabetes. Data from the National Diabetes Inpatient Audit suggest that people with diabetes experience avoidable prescription errors such as wrong insulin, incorrect doses and omitted doses. These errors result in increased length of stay and harm to

the patient. Many of the errors occur due to deficiencies in knowledge. Our aim was to reduce prescription errors and improve health care professionals’ knowledge by introducing the following initiatives: why (1) redesign of the diabetes prescription chart; and (2) implementing a root cause analysis Akt inhibitor prescription error pathway which involves a targeted approach to education for the individual who made the error. Following introduction of the changes to the insulin prescription chart, data from our participation in the National Diabetes Inpatient Audit reported that prescription errors were reduced from 65% to 14% and management errors from 40% to 14% from 2009 to the beginning of 2012. The results of the internal audit during

2012–2013 demonstrated a further reduction in prescription/management errors to 2% following the introduction of the root cause analysis pathway. The changes have demonstrated a significant reduction in prescription errors and an increased awareness of diabetes following the targeted approach to education. Copyright © 2013 John Wiley & Sons. “
“The incidence of type 1 diabetes and type 2 diabetes in children and adolescents is rising. The associated public health burden is substantial with major implications for those involved in planning health care provision at all levels. The aetiology of diabetes in this age group is poorly understood, although both genetic and environmental factors are likely to be involved. Clinicians involved in the management of diabetes in the young in the Northern Region have wanted to establish a diabetes registry for more than two decades.

Introns were detected in the cox1, cox2, nad5, rns and rnl genes. All of these are type I introns, except for the single type II intron in rns. All type I introns contained endonuclease-like gene sequences with the conserved LAGLIDADG motif, except for the first intron in the cox1 gene, which had the GIY-YIG motif. The endonuclease in cox1 intron-12 appears to be truncated and does not have the full LAGLIDADG domain. Of the genes found in the mitochondrial genome of T. cingulata, the structure of cox1 is the most complex. Of the 16 exons that

make up the cox1 gene, five are smaller than 20 nt long, with the smallest two being only 11 nt. All 15 introns have at least one ORF larger than 100 codons. ORFs encoding endonuclease-like sequences BIBF 1120 mouse were also seen in all other introns, except for intron-1 of cox2. The reading frames of the exons 1 and Avasimibe in vivo 2 of nad5 continue well beyond the predicted splice sites into the respective introns. These extended reading frames also encode endonuclease-like sequences within an ORF (Fig. 1). While the coding regions have been well conserved among the Agaricomycotina

and to a lesser extent with U. maydis, the introns show less similarities (Fig. 1). Trametes cingulata intronic ORFs show greater sequence similarity to P. ostreatus and M. perniciosa than to the more distantly related U. maydis. Schizophyllum commune and C. neoformans do not have introns in the same genes as T. cingulata. The DNA and RNA polymerases dpo and rpo, which have been reported in P. ostreatus and M. perniciosa, are not present in the T. cingulata mitochondrial genome nor were they annotated or obvious in the S. commune, C. neoformans or U. maydis mitochondrial genomes. The 25 identified tRNAs genes

represent all 20 amino acids and include three copies encoding tRNAMet and two each of tRNAArg, tRNASer and tRNALeu. Single genes encode the other 16 tRNAs. We analyzed codon usage for the 15 protein-encoding annotated genes (Supporting Information, Table S1) and found that all of these genes use TAA Amylase as the stop codon, except for nad5, which uses TAG. nad5 is also the only gene that uses GAG as a codon for glutamic acid and AGG for arginine, which is otherwise encoded exclusively by AGA. Other codons for arginine, CGG, CGT and CGC, are not used. The glycine codon GGC is also not used. At least one of these four otherwise unused codons is used one or more times in all five of the unidentified ORFs, lending additional support to the hypothesis that these ORFs are not expressed genes. The alternate codon for tryptophan TGA that differs from the standard codon table is not used either as a codon for tryptophan or to represent a stop codon in the 15 protein-encoding annotated genes. However, it is present twice in ORF111 and once in ORF158. Nad4L is the only gene that uses AAG to code for lysine and does it only at one position. Only 13% of the codons for tyrosine use TAC, with the rest using TAT.