Both auto body repair and bakery workers who reported skin symptoms were consistently and significantly

more likely to report work-related and non-work-related respiratory symptoms. These findings are comparable with results of Lynde et al. (2009) who showed that male cleaners with a skin rash were more likely to report respiratory symptoms, particularly work-related respiratory symptoms. The prevalence of skin symptoms reported in auto body shop workers and bakery workers is similar to previous studies of skin outcomes in these populations. Randolph et al. (1997) reported that 32 % of HDI-exposed spray painters reported hand dermatitis, while Daftarian et al. (2002) found 35 % of TDI-exposed workers to have skin symptoms. Cullinan et al. (2001) found that 11 % of bakery and flour mill workers had skin symptoms. Steiner et al. (2011) reported that 19 % of all bakers and 31 % of high-risk (higher likelihood of exposure) selleck kinase inhibitor bakers reported at least one skin symptom in the last 12 months. Previous research supports that self-reported skin symptoms are predictive of skin disease. Proteasome inhibitor However, some results suggest that self-reported skin symptoms may overestimate (Smit et al. 1992; Lynde et al. 2009) or underestimate (Holness et al. 1995) the prevalence of disease when

compared with a physician examination. The use of picture-based questionnaires and self-reported doctor-diagnosed dermatitis may provide a prevalence estimate closer to that of physician diagnoses, but may also underestimate prevalence (Smit et al. 1992). Skin symptoms may be due to irritant or different immunologic (Type I or Type IV) mechanisms. Though it is possible to differentiate Amylase between these outcomes in the clinical setting, it is not possible to differentiate using symptoms reported on the questionnaire alone. The strong relationship between

wheat-specific IgE and work-related itchy skin supports a role for the IgE-mediated (Type I) allergy in the development of work-related skin symptoms in bakery workers. Parallel results for respiratory symptoms (Supplemental Material) also demonstrate strong relationships between wheat-specific IgE and both asthma-like symptoms and work-related chest tightness. It is not possible to model the potential role of Type IV allergy or irritant mechanisms in symptom development in this study. The bell-shaped (non-linear) distribution observed for non-atopic auto body shop workers in the smoothing splines (Fig. 1) may be the result of a healthy worker effect, with fewer symptomatic subjects at the higher exposure levels. A healthy worker effect was also suggested by the negative association between exposure and atopy in both the auto body shop and bakery workers (Table 2). The prevalence of work-related allergen-specific sensitization was five times higher in bakery workers (11 %) compared to auto body shop workers (2 %).

5 mg/l ampicillin and 5% lglycerol; G – LB with 0.06 mg/l cefotaxime and 5% l glycerol; H – LB with 1.5 mg/l tetracycline and 5% glycerol. Discussion Plaque development has been the subject of several recent reviews [28–32]. Plaque size seems to be directly proportional to burst size, phage adsorption constant and the diffusion of phages in the medium and inversely proportional to the latent period, each factor contributing

differently [25, 28, 29]. A decrease in the latent period and an increase in burst size has been observed in the presence see more of antibiotics [19–25]. The enhancement of phage production by antibiotics is reported to be due to bacterial filamentation [25]. Krueger et al. observed that penicillin-treated S. aureus produced filaments three times the diameter of normal bacteria [19] and enhanced phage development. Hadas et al. also found that bacterial cells exposed to this

antibiotic were 4-fold larger and the yield of phage production was enhanced by an equal amount. Burst size also increases in parallel with DNA content but not with DNA concentration [23]. Thus, it seems that cell size rather than metabolic rate is a major influence on phage development in the presence of antibiotics. Further experiments showed that the rate of phage production is proportional to the amount per cell of the protein synthesizing system (PSS) at the time of infection and is not limited by cell size or DNA composition [23, 33]. In fact, larger faster-growing cells contain proportionally more PSS leading www.selleckchem.com/products/INCB18424.html to higher phage production. Thus, cell size does not play a primary role in increasing phage production but has an

indirect effect by increasing PSS. As a result, because some antibiotics trigger the SOS system, the bacterial cells will divide poorly, increasing their size and resulting in cell filamentation, which in turn will increase their PSS content, thus enabling an increase in phage production. From this we can conclude that any stimuli that increase PSS content click here will increase phage production and plaque size, and such stimuli may act indirectly by filamentation or inducing the SOS response. This seems to explain why glycine stimulates plaque formation, as in the work presented by Lillehaug. This amino acid has been shown to weaken the bacterial cell wall, which induces the SOS response and consequently increases the PSS content. This fact has remained hitherto unexplained [10, 23, 33]. As a consequence, any substance or condition (e.g. agitation or temperature) that directly or indirectly stimulates an increase of PSS is able to increase phage production and thus plaque size. The adsorption rate is also influenced by antibiotics: it is directly proportional to cellular surface area and therefore increases when cells are subjected to some antibiotics, as observed by Hadas et al. (1997) [23, 33].

2009). Fig. 2 The three-dimensional matrix describing how research is structured in LUCID In sum, the present scientific understanding

signals that sustainability challenges are multi-scalar, multi-faceted and strongly interrelated in complex ways that require integrated solutions across scales and domains (Kates et al. 2001). In consequence, attempts to handle urgency, complexity, interconnectivity and uncertainty may trigger difficult dilemmas and conflicting concerns in society. We, therefore, identify a sequence of stages included in the matrix (see Fig. 2 left side) for how to socially recognise, act upon and learn about sustainability challenges as interconnected problem syndromes: Scientific understanding Society creates and establishes structures

to communicate, BTK inhibitor ic50 beyond scientific communities, the natural scientific knowledge on causes and www.selleckchem.com/products/AG-014699.html magnitudes of the impacts of a particular sustainability challenge, like climate change3. Sustainability goals Society formulates and negotiates social goals, for one or multiple challenges, in political dialogues between society and science4. Sustainability pathways and strategies Society takes political decisions on pathways and strategies to fulfil the goals5. Implementation Society implements strategies, policies and measures while simultaneously initiating social learning processes to evaluate implementations and Tideglusib outcomes6. If sustainability science speaks with the Anthropocene vocabulary, then it means that sustainability challenges can only be met when the fundamental interconnections between nature and society are studied in more systematic, integrated and flexible ways (Kates et al. 2001; Ostrom 2009; Rockström et al. 2009). The strong tradition of separating natural and social sciences

in academia has resulted in an inadequate understanding of nature–society interactions and the integrated dynamics of the ‘Earth System’ as a whole (Schellnhuber 1999; Steffen et al. 2004). We, therefore, suggest that researchers who collaborate across disciplines to adopt integrated approaches for overcoming the divide also seek to maintain reflective, reflexive and critical approaches to the Anthropocene imagery and to scientific representations in which nature and society are integrated as a whole (Lövbrand et al. 2009). Old and new concepts in sustainability science The structuring of the research field of sustainability science must draw upon scholarly work from a range of disciplines. Such a broad basis provides a crucial starting point for understanding theoretical and empirical multiplicities and addressing the urgency of sustainability challenges. This section describes the scientific connectivity. We proceed from the assumption that social and natural systems are characterised by complexity, non-linearity, self-organisation and strong interlinkages.

Cell 1990,63(5):933–40.PubMedCrossRef 13. Freije JM, Blay P, MacDonald NJ, Manrow RE, Steeg PS: Site-directed mutation of Nm23-H1. Mutations lacking motility suppressive capacity upon transfection are deficient in histidine-dependent protein phosphotransferase pathways in vitro. J Biol Chem 1997,272(9):5525–32.PubMedCrossRef 14. Ma D, McCorkle JR, Kaetzel DM: The metastasis suppressor NM23-H1 possesses 3′-5′ exonuclease activity.

J Biol Chem 2004,279(17):18073–84.PubMedCrossRef 15. Kaetzel DM, Zhang Q, Yang M, McCorkle JR, Ma D, Craven RJ: Potential roles of 3′-5′ exonuclease activity of NM23-H1 in DNA repair and malignant progression. J Bioenerg Biomembr check details 2006,38(3–4):163–7.PubMedCrossRef 16. Lee HY, Lee H: Inhibitory activity of Nm23-H1 on invasion and colonization of human prostate carcinoma cells is not mediated by its NDP kinase activity. Cancer Lett 1999,145(1–2):93–9.PubMedCrossRef 17. Jung S, Paek YW, Moon KS, Wee SC, Ryu HH, Jeong YI, Sun

HS, Jin YH, Kim KK, Ahn KY: Expression of Nm23 in gliomas and its effect on migration and invasion in vitro. Anticancer Res 2006,26(1A):249–58.PubMed 18. Fang Z, Yao W, Xiong Y, Zhang J, Liu L, Li J, Zhang C, Wan J: Functional elucidation and methylation-mediated downregulation of ITGA5 gene in breast cancer cell line MDA-MB-468. J Cell Biochem 2010,110(5):1130–41.PubMedCrossRef 19. Sosnoski DM, Emanuel BS, Hawkins AL, van Tuinen P, Ledbetter DH, Nussbaum RL, Kaos FT, Schwartz E, Phillips D, Bennett JS, Fitzgerald LA, Poncz M: Chromosomal CDK inhibitor localization of the genes for the vitronectin and fibronectin receptors alpha subunits and for platelet glycoproteins IIb and IIIa. J Clin Invest

1988,81(6):1993–8.PubMedCrossRef 20. Qin L, Chen X, Wu Y, Feng Z, He T, Wang L, Liao L, Xu J: Steroid receptor coactivator-1 upregulates integrin α5 expression to promote breast cancer cell adhesion and migration. Cancer Res 2011,71(5):1742–51.PubMedCrossRef 4-Aminobutyrate aminotransferase 21. Williams SJ, White BG, MacPhee DJ: Expression of α5 integrin ( Itga5 ) is elevated in the rat myometrium during late pregnancy and labor: Implications for development of a mechanical syncytium. Biol Reprod 2005,72(5):51114–1124.CrossRef 22. Rozen S, Skaletsky H: Primer3 on the WWW for general users and for biologist programmers. Methods Mol Biol 2000, 132:365–86.PubMed 23. Fan S, Meng Q, Gao B, Grossman J, Yadegari M, Goldberg ID, Rosen EM: Alcohol stimulates estrogen receptor signaling in human breast cancer cell lines. Cancer Res 2000,60(20):5635–9.PubMed 24. Zhu Y, Lin H, Li Z, Wang M, Luo J: Modulation of expression of ribosomal protein L7a (rpL7a) by ethanol in human breast cancer cells. Breast Cancer Res Treat 2001,69(1):29–38.PubMedCrossRef 25. Vaeth PA, Satariano WA: Alcohol consumption and breast cancer stage at diagnosis. Alcohol Clin Exp Res 1998,22(4):928–34.

In addition, cell viability was significantly lower in cells subjected to nanoscale photosensitizer-mediated PDTs than in cells treated with the conventional. In the conventional Photosan group, cells incubated for 2 h at 10 J/cm2 cell showed

a gradual decline in viability as Photosan concentrations increased from 0 to 20 mg/L, with significant differences in cell viabilities at different concentrations. At 20 mg/L, no statistically significant differences in cell viability were observed between conventional and nanoscale Photosan treatments. HepG2 cell-treated nanoscale Photosan showed a different pattern: cell viability declined as photosensitizer concentrations increased from 0 to 5 mg/L and stabilize thereafter (Figure 1B). According to these findings, 10 and 5 mg/L were used in subsequent experiments selleck chemical for conventional and nanoscale photosensitizers, PLX4032 datasheet respectively. At fixed photosensitizer incubation times and concentrations, cell viability was significantly affected by light doses. In addition, cell viability was significantly lower in cells subjected to nanoscale photosensitizer-mediated PDTs than in cells treated with the conventional. In the conventional Photosan group, cells

incubated for 2 h in the presence of 5 mg/L photosensitizer showed a gradual decline in cell viability as light doses increased from 2.5 to 10 J/cm2, with significant differences at different light doses. In cells treated with nanoscale Photosan, significant differences in cell viability were observed between exposure at different light intensities, Rutecarpine from 0 to 5 J/cm2, with no significant difference in cell viability observed thereafter (Figure 1C). Accordingly, 10 and 5 J/cm2 were used in further experiments

for conventional and nanoscale photosensitizers, respectively. Effects of conventional and nanoscale photosensitizers PDT on human hepatoma cell apoptosis Flow cytometry was used to quantitate apoptosis rates in human hepatoma cells submitted to conventional Photosan-based PDT or nanoscale Photosan-based PDT. Group a cells were the blank control; group b cells were treated with 5 mg/L nanoscale Photosan for 2 h at 5 J/cm2; group c cells received 5 mg/L conventional Photosan for 2 h at 5 J/cm2; group d cells were treated with 10 mg/L conventional Photosan for 4 h at 10 J/cm2. As shown in Figure 2, apoptosis rates for groups a, b, c, and d were 17.14%, 80.33%, 40.66%, and 72.33%, respectively. The treatment groups (groups b, c, and d) significantly differed from the control group a (P < 0.05). Total apoptosis rates were similar in groups b and d (P > 0.05), and significantly higher in group b compared with group c (P < 0.05). Flow cytometry data further confirmed the cytotoxic effects of PDT as detailed above.

melanogaster w1118 [23]. In our view, the

electron-dense LDK378 structures, which we revealed at the periphery of region 1 of the germarium, are presumably autophagosome encapsulated dying Wolbachia. A supporting line of evidence came from Wright and Barr [37], who on the basis of their observations on degenerating germaria cysts from mosquitoes Aedes scutellaris suggested that these structures represented degenerating Wolbachia. Cell fragments containing dying bacteria and autophagosomes and appearing as numerous smaller puncta in regions 2a/2b and 1 of the germarium may represent autophagy, not apoptosis. This appears plausible when recalling that AO stains not only apoptotic cells, also lysosomes [38]. TUNEL did not reveal such puncta in these regions. The possible role of the Wolbachia strain wMelPop in programmed cell death in region 2a/2b of the germarium Our current estimates of apoptosis in region 2a/2b of the germarium from the ovaries of the uninfected D. melanogaster w1118T raised on standard food are consistent with those reported elsewhere [14]. It is of interest that apoptosis level in the germaria decreased in D. melanogaster w1118T , but not FK506 order in D. melanogaster Canton ST after transfer to rich food. This may be indicative of differences in sensitivity to changes in food composition between different fly stocks. AO- and TUNEL staining demonstrated that the virulent Wolbachia strain wMelPop increased

the percentage of germaria containing apoptotic cells in D. melanogaster w1118 ovaries, while wMel strain was without such an effect. The effect of wMelPop on cystocytes in ovaries was observed in flies maintained on standard and rich food. Evidence was provided that the effect of Wolbachia on D. melanogaster is not general, to being rather specific to the pathogenic strain wMelPop. What pathways may be envisaged for the Wolbachia strain wMelPop caused increase in the number

of germaria whose cysts undergo apoptosis? On the one hand, bacteria may have a direct effect on germline cells (Figure 7A, B). In fact, one of 16 cyst cells becomes the oocyte, the other 15 differentiate into nurse cells in region 2a of the germarium. This is associated with transport of 15 centrioles into the pre-oocyte, where the microtubule-organizing center forms [39, 40]. Wolbachia distribution is dependent upon microtubules during oogenesis and bacteria show mislocalization in the egg chambers treated with colchicine which causes depolymerization of microtubules [41]. Evidence has been obtained indicating that Wolbachia are evenly distributed throughout the oocyte and nurse cells during stages 1-2 of oogenesis, becoming concentrated at the oocyte anterior during stages 3-6 [41]. With this in mind, the high levels of Wolbachia in cystocytes during differentiation into oocyte and nurse cells in region 2a of the germarium may possibly lead to impairment at the structural and/or molecular level, the cyst may undergo apoptosis as a consequence (Figure 7B).

Participants Insurance physicians A total of 100 IPs who assess claimants for long-term disability

benefits were randomly selected from a pool of 566 IPs who work for the Institute for Employee Benefit Schemes (UWV) in the Netherlands. This semi-governmental organization employs all IPs who perform statutory assessments of claimants for long-term disability benefit in the Netherlands. To test the hypothesis that 66% of the IPs conclude that FCE information has a complementary value for the assessment of physical work ability, under the assumption of the H0 hypothesis of 40% (Wind et al. 2006), click here 28 IPs had to be included (α = 0.05, β = 0.8). All participating IPs signed an informed consent form. Claimants Each IP gave information

about the study to a number of MSD claimants who were due to be assessed in the context of long-term disability benefit claims. The information packet included an application form that the claimant could fill out and send directly to the researchers. The claimants could also indicate that they did not wish to participate and explain why (though they were not obliged to give any reason). The first claimant seen by a given IP who agreed to take part in the study underwent an FCE assessment after signing an informed consent form. The claimant received a copy of the FCE report. The Medical

Ethical Committee of the Academic BGB324 mouse Medical Center, Amsterdam, approved the study. The study period was from November 2005 to February 2007. Procedure Each IP was asked to assess the physical work ability in accordance with the statutory rules for the claimant who had volunteered to participate in the study. After receiving the report of the FCE assessment from the FCE provider, this report very was presented to the IP in combination with his own report in the patient’s file. After reading the FCE report, the IP was requested to fill in a questionnaire in which he gave his opinion of the complementary value of the FCE information and stated whether the information led him to change his initial assessment. The statutory assessment of the claimant for the purposes of the disability benefit claim was based on the IP’s initial judgement, i.e., the FCE information had no influence on this statutory assessment (Fig. 1). Fig. 1 A flow diagram of the study design FCE test The FCE instrument used in this study was the Ergo-Kit. This FCE is comprised of a battery of standardized tests that reflect work-related activities. The standard protocol, containing 55 tests, was performed by certified raters and took approximately three hours to complete.

No less than ‘true’

woodlands, they may be rare or residual as such, and host species of Community interest. Some types of wood-pasture are famous for their old trees, even more so than in other types of used woodlands. The proportion of deadwood may also be high. Some are ‘ancient’ in that wood-pasture has been practised through centuries and, although no records of any significant age exist, some may PI3K inhibitor not have been much changed over time, hence we may even call it a ‘sustainable’ kind of management. Nevertheless, woodlands eligible for the Natura 2000 network are supposed to show typical woodland undergrowth, i.e., mesophytic and

shade-tolerant, and a “high degree of naturalness”. However, the structure of wood-pastures is man-made, and if criteria and definitions of forest habitats were applied, even high-quality wood-pasture sites, with natural regeneration in the presence of grazing, could only be assessed with an unfavourable conservation status. Nevertheless, the habitat type 9070 (Fennoscandian wooded pastures), clearly a type of wood-pasture, selleck screening library Protein tyrosine phosphatase inconsistently has become a forest habitat type. Only few other wood-pasture habitat types have been recognized at

all in Annex I of the Habitats Directive, under the headings of ‘Submediterranean and temperate scrub’ (5130: Juniperus communis formations on heaths or calcareous grasslands) ‘Mediterranean arborescent matorral’ (5210: Arborescent matorral with juniper), ‘Sclerophyllous grazed woodlands’ (6310: Dehesas with evergreen oaks), ‘Mesophile grasslands’ (6530: Fennoscandian wooded meadows). A few types of ‘Temperate heath and scrub’, notably 40A0 (Subcontinental peri-Pannonic scrub) and 40C0 (Ponto-Sarmatic deciduous thickets) also belong here. What is missing? Tables 2 and 3 shows the relation between Annex I habitat types and European wood-pasture types. Only few wood-pasture types fully match Annex I habitat types. Most wood-pasture types are somehow represented under certain forest habitat types. In fact, some of the forest habitat types exist to date only as pasture woodlands. Clearly, this arrangement is unsatisfying and conflicting.

62 patients from the topiroxostat group and 60 patients from the placebo group were included in the intent-to-treat population (Fig. 1). Among intent-to-treat population, the serum urate was not measured in two patients of the topiroxostat group at the point of discontinuation of the study. Fig. 1 Patient distribution. Asterisk discontinuance criteria (serum urate <118.96 μmol/L) The baseline characteristics of the two treatment groups were similar, except for a lower proportion of patients with complication of diabetes in the topiroxostat group (29.0 vs. 41.7 %;

P = 0.1442) (Table 1). Table 1 Summary of the baseline characteristics of the intent-to-treat population Variable Topiroxostat (n = 62) Placebo (n = 60) Inhibitor Library high throughput P value Age (years) 62.5 ± 8.8 64.6 ± 8.1 0.18503 Sex (male/female) 53/9 56/4 0.16001 Body mass index (kg/m2) 25.75 ± 4.45 25.51 ± 3.10 0.72033 Serum urate (μmol/L) 503.80 ± 73.76 503.80 ± 76.13 0.99683 Duration of hyperuricemia (years) 9.65 ± 11.23 9.51 ± 9.24 0.94723 Diabetic nephropathy, n (%) 14 (22.6) 19 (31.7) 0.25871 Chronic glomerulonephritis, n (%) 3 (4.8) 5 (8.3) 0.48752 Nephrosclerosis, n (%) 10 (16.1) 12 (20.0) 0.57821 Diabetes, n (%) 18 (29.0) 25 (41.7) 0.14421 eGFR (mL/min/1.73 m2) 49.40 ± 8.93 48.89 ± 8.51 0.74343 ACR (mg/g) geometric mean (IQR) 41.71 (12.53–132.70) 29.92 (11.05–48.15) 0.23413 SBP (mmHg) 135.2 ± 17.3

Neratinib 134.6 ± 20.0 0.86033 DBP (mmHg) 84.8 ± 11.8 84.1 ± 11.6 0.74763 Serum Adiponectin (μg/mL) 9.29 ± 5.47 10.30 ± 6.45 0.35593 RAA blockers, n (%) 38 (61.3) 31 (51.7) 0.28371 eGFR estimated glomerular

filtration rate, ACR urinary albumin-to-creatinine ratio, SBP systolic blood pressure, DBP diastolic blood pressure, RAA blockers use of angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, aldosterone blockers, or renin inhibitor 1 χ 2 test, 2 Fisher’s exact test, 3 Student’s t test Percent change of the serum urate The percent change of the serum urate from the baseline to the final visit Pregnenolone was significantly higher in the topiroxostat group than that in the placebo group (topiroxostat: −45.38 ± 21.80 % (n = 60), placebo: 0.08 ± 9.92 % (n = 60), between-group difference: −45.46 %; 95 % confidence interval (CI) −39.33 to −51.58, P < 0.0001) (Fig. 2a). Fig. 2 Percent change of the serum urate levels and proportion of patients with serum urate levels ≤356.88 μmol/L at the final visit (intent-to-treat population). a Percent change of the serum urate level from the baseline to the final visit. Results are expressed as mean ± SD. b Proportion of patients with serum urate levels ≤356.88 μmol/L at the final visit. Results are expressed as percentages and its 95 % CIs. Two patients of the topiroxostat group were withdrawn without measurement of the serum urate levels during the study.

YitA GS-1101 nmr and YipA persist for several hours following a growth temperature shift to 37°C YitA and YipA levels over time following a temperature shift from 22°C to 37°C was determined by Western blot analysis. YitA and YipA synthesized by KIM6+ (pCR-XL-TOPO::yitR) following growth in BHI at 22°C were still present 7 hours after an upshift to 37°C (Figure 4, lanes 5, 8, 11, 14, and 18). After 9 hours, a slight reduction

in YitA and YipA protein was seen in the 37°C culture compared to the matched culture maintained at 22°C (Figure 4, lanes 21 and 20, respectively). After 24 hours, there was a significant decrease in detectable YitA and YipA (Figure 4, lane 24) in the 37°C culture. After 30 hours at 37°C, only a small quantity of YitA remained and no detectable YipA (Figure 4, lane 27). Figure 4 YitA and YipA proteins persist in Y. pestis for at least 9 hours after transfer to 37 °C . Y. pestis KIM6+ (pCR-XL-TOPO::yitR) (lanes 5, 8, 11, 14, 18, 21, 24, and 27) and KIM6+ΔyitA-yipB (pCR-XL-TOPO::yitR) (lanes 3, 6, 9, 12,

15, 19, 22, 25, and 28) were grown overnight at 22°C and subsequently transferred to 37°C for the indicated amount of time prior to sample collection. A matched KIM6+ (pCR-XL-TOPO::yitR) was maintained at 22°C as a positive reference control (lanes 2, 4, 7, 10, 13, 17, 20, 23, and 26). T0 = initial time point, T(x) = x hours at 37°C. Panels show Western blots probed with anti-YitA, anti-YipA, or anti-Ail (sample loading control) antiserum. Evidence for post-translational

processing of YipA GBA3 Two forms of YipA were typically detected by Western Navitoclax blot: the predicted full-length protein at ~106 kDa and a smaller protein of ~73 kDa, with the smaller form often predominating (Figures 2, 3, 4). To determine which of the bands detected using anti-YipA serum correspond to the N-terminal region and the C-terminal region of YipA, Y. pestis strains containing translational fusions of mature β-lactamase (~28.9 kDa) to the C-terminus of YitA or YipA were constructed (Figure 1B). After overnight growth at 22°C, Y. pestis YitA-β-lactamase and YipA-β-lactamase with or without plasmid pCR-XL-TOPO::yitR were assayed by Western blot. YitA-β-lactamase was detected by anti-YitA serum as a single band at ~123 kDa (due to the addition of the mature β-lactamase) with a light smear of smaller bands (Figure 5A, lane 2), whereas wild-type YitA was detected around 95 kDa (Figure 5A, lane 4). Anti-β-lactamase antibody also detected full length YitA-β-lactamase at ~123 kDa as a prominent band and a smear of several smaller bands (Figure 5C, lane 2). Figure 5 Characterization of post-translational processing of YipA. KIM6+ (pCR-XL-TOPO::yitR) with the C-terminus of YitA (Lane 2) or YipA (Lane 4) tagged with mature β-lactamase were grown overnight at 22°C in BHI broth.