The Capture the Fracture Campaign provides all necessary evidence, international selleck chemical standards of care, practical resources and a network of innovators to support colleagues globally to close the secondary prevention care gap. We call upon those responsible for fracture patient care throughout the world to implement Fracture Liaison Services as a matter of urgency. Acknowledgments The authors would like to thank Gilberto Lontro (Senior Graphic Designer, IOF),

Chris Aucoin (Multimedia Intern) and Shannon MacDonald, RN (Science Coordinator, IOF) for their excellent and many contributions to development of the Capture the Fracture Campaign. We are also very grateful to the following colleagues throughout the world who have provide invaluable support in the development of the Best Selleckchem Saracatinib Practice Framework: Dr. Andrew Bunta (Own the Bone, American Orthopaedic Association, USA), Dr. Pedro Carpintero (selleck chemicals University Hospital Reina Sofia, Cordoba, Spain), Dr. Manju Chandran (Singapore General Hospital, Singapore), Dr. Gavin Clunie (Addenbrookes Hospital, Cambridge, UK), Professor Elaine Dennison (University of Southampton, UK), Ravi Jain (Osteoporosis Canada), Professor Stephen Kates (University of Rochester Medical Center, USA), Dr. Ambrish Mithal (Medanta Medicity, Gurgaon, India), Dr. Eric Newman (Geisinger Health System, USA), Dr. Marcelo Pinheiro (Universidade

Federal de São Paulo, Brazil), Professor Markus Seibel (The University of Sydney at Concord, Australia), Dr. Bernardo Stolnicki (Federal Hospital Ipanema, Brazil), Professor Thierry Thomas (Groupe de Recherche et d’Information sur L’ Ostéoporose [GRIO], France), Dr. Jan Vaile (Royal Prince Alfred Hospital, Sydney, Australia), Dr. John Van Der Kallen (John Hunter Hospital, Newcastle, Australia).

Conflicts of interest None. not Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. Open AccessThis article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. Appendix. Capture the Fracture Best Practice Framework The 13 Capture the Fracture Best Practice Standards are: 1. Patient Identification Standard   2. Patient Evaluation Standard   3. Post-fracture Assessment Timing Standard   4. Vertebral Fracture Standard   5. Assessment Guidelines Standard   6. Secondary Causes of Osteoporosis Standard   7. Falls Prevention Services Standard   8. Multifaceted health and lifestyle risk-factor Assessment Standard   9. Medication Initiation Standard   10. Medication Review Standard   11. Communication Strategy Standard   12. Long-term Management Standard   13.

Such models allow independent testing of different experimental treatments on both gut microbiota

Momelotinib in vivo composition and metabolic activity within a single experimental period, using the same microbiota under controlled environmental conditions, which are designed to simulate the proximal, transverse and distal colon of healthy and infected subjects [9–14]. More recently, a three-stage in vitro colonic fermentation model of Salmonella infection in child colon was used to assess the effects of probiotic and prebiotic treatments on gut microbial behavior and on S. Typhimurium infection [15]. The activity of microcin B17-producing Escherichia coli L1000 wt [16] and bacteriocinogenic Bifidobacterium thermophilum RBL67, both exhibiting strong anti-Salmonella activity in simple in vitro tests [17, 18], as well as the microcin B17-negative mutant strain MccB17-, were tested in two three-stage models inoculated with the same fecal inoculum. When added to the colonic model, E. coli L1000 unexpectedly stimulated Salmonella growth in all reactors independently of the microcin B17-phenotype, partly due to a low colonization of the strain in the complex intestinal environment. In contrast, thermophilicin RBL67-producing Bifidobacterium thermophilum RBL67 revealed

high competitiveness and colonized at high levels but did not reduce Salmonella counts, most likely a function of the presence of a very high Salmonella population in the in vitro model prior to probiotic addition. PARP inhibitor Most data available on the mechanistic effects of probiotics on the host are derived from in vitro studies with

intestinal cells [19]. Such models have also been used to investigate bacterial interactions with the intestinal epithelium during enteric infection [20]. Salmonella these pathogenesis, for example, has been studied in pure selleck screening library cultures using epithelial Caco-2 and HT-29 cell models [21, 22], both of which lack the ability to produce mucus. The mucus-secreting HT29-MTX cell line however, represents more accurate physiological conditions of the gastrointestinal tract for investigating pathogenic behavior during infection, as the presence of mucus has been shown to enhance pathogenicity of pathogens such as Campylobacter jejuni [23]. All interaction studies of pathogens and probiotics with intestinal cells have been performed with simple systems of either pure or mixed cultures. Microbe cell interactions are however different when tested in the presence of a complex gut microbiota [24, 25]. Gut metabolites such as SCFAs affect epithelial cell metabolism, turnover and apoptosis [26] but may also enhance virulence (e.g. S. Typhimurium), by inducing an acid tolerance response or increasing expression of porins [27]. To our knowledge, the effects of an infected gut microbiota, including its metabolites and probiotic treatment on intestinal cells has not been previously reported.

8006. Cmm strains from the recent epidemics in Belgium in 2010–2012 showed identical MLVA haplotypes which suggests that a clonal population was responsible for these outbreaks. The presence of the same MLVA haplotypes of Cmm strains from 2011 and 2012 could mean that bacteria persisted in the used equipment, devices or soil and induced the outbreaks in the following years. Population of Belgian strains isolated from 2010–2011 is epidemiologically related to at least two French strains that exhibited the same

MLVA haplotype. Moreover, based on minimum spanning tree, Belgian strains were found to be evolutionary related to the French strain PD 5749. When MLVA data was analyzed taking into account differences in the number of repeats it appeared that two French and two Spanish strains were found to have a similar MLVA find more haplotype to the group Alvocidib research buy of Belgian strains from 2010–2012 suggesting that there might be a common origin of these strains (Additional file 1: Figure S1). It is worth mentioning that the strain

ES 2686.1 isolated in Spain in 2002 was linked to outbreaks of Cmm in 2002–2007 in Canary Islands [6]. Two French strains isolated in 2010 showed the same MLVA haplotype as strains from recent Belgian outbreaks which may imply that the contaminated material was spread also in France. Different MLVA patterns between strains from the recent Belgian outbreaks of 2010–2012 and Belgian strains isolated previously support our hypothesis about a novel introduction, presumably originating from a single lot of seeds or contaminated tomato seedlings. Remarkably, all

Belgian Cmm strains from 2010–2012 MK 2206 (Table 1), were purchased from the same nursery. In this study, VNTR loci were chosen to be longer than or equal to 20 bp to simplify the interpretation of the results from an agarose gel and to allow performing the analysis in standard laboratories not equipped in sophisticated tools (fragment analyzer or sequencer) required to analyze small (a few nucleotides) differences in an amplicon size. Shorter repeats are represented in a higher number of copies and are more likely to be polymorphic [49]. However, many studies showed successful application of longer repeats which gave satisfactory resolution and discriminatory power [16, 50]. Interleukin-2 receptor Moreover, in silico analysis of tandem repeats in the Cmm genome NCPPB 382 revealed only a few short repeats (6–8 bp) that had remarkably higher number of copies (around 10 copies).These microsatellite loci might be investigated in the future and combined with currently available MLVA scheme. MLVA can provide phylogenetic information even with a limited number of loci [51]. MLVA assays are relatively robust [17, 52] but as any other technique they have their limitations. In MLVA, a need to develop a new set of loci for every species or serovar under investigation might be necessary.

PCR band intensities were expressed as Optic Density (OD) normalized for β-actin expression. Data are OICR-9429 solubility dmso presented as a ratio compared with the respective controls, which received an arbitrary value of 1 in each experiment.

Statistical analysis Data are presented as mean ± SEM (standard error of the mean). The normality of distribution of all parameters was checked with the Kolmogorov-Smirnov test and by the homocedasticity test (Bartlett criterion). All variables presented normal distribution and homocedasticity, thus the two-way ANOVA test was used, (taking into consideration the variables exercise × oat bran enriched diet) and when the difference presented was significant, Tukey’s post hoc test was used. A significance level of p ≤0.05 was used for all comparisons. The software package used was SPSS for Windows version 10.0. Results Time to Exhaustion The time to exhaustion SIS3 clinical trial of the EX-O group

was 515 ± 30 minutes and 425 ± 30 for the EX group (p = 0.034). This represented a 20% higher exhaustion time for the EX-O group when compared with the EX group. Figure 1 Figure 1 Time to exhaution on experimental groups. a = statistical difference to exhaution group (EX) Corticosterone and Cytokine Concentrations Corticosterone levels were significantly elevated after exercise to exhaustion compared with the control group. The EX group DZNeP order presented significantly higher corticosterone levels compared with the EX-O group, (p = 0.039) (figure 2). Similarly, after exercise IL-6 was increased in EX and EX-O compared with the control. The EX-O group showed lower levels of IL-6 compared with the EX group, (p = 0.001) (Table 2). The serum levels of TNF-α were significantly decreased after exercise in the EX and EX-O groups compared with the control group. However, no statistically significant differences were observed between EX and EX-O for TNF-α serum levels (Table 2). IL-10

serum levels were increased after exercise compared with the control group, and EX presented significantly Glutamate dehydrogenase higher levels of IL-10 as compared with EX-O (p = 0.032) (Table 2). Figure 2 Corticosterone levels in experimental groups. a = statistical difference to control group b = statistical difference to EX group Table 2 Plasma cytokine concentration in experimental groups. (pg/ml) C EX EX-O IL-6 11.2 ± 17 163 ± 2.7* 127 ± 3.6*# IL-10 50.5 ± 9.4 328.5 ± 78* 84.3 ± 53.4*# TNF-a 31.1 ± 1.34 5.58 ± 1.0* 2.6 ± 0.4* Values are presented as mean ± standard error of the mean. Control (C), exhaustion (EX) and exhaustion treated with oat bran (EXO) groups, (n = 9), p ≤ 0.05. IL-6 = interleukin-6; IL-10 = interleukin-10; TNF-a = Tumor necrosis factor-a. *Statistically significant difference compared with C group; #statistically significant difference compared with EX group.

For example, in male workers of this study, neither low job control nor high job demand was significantly associated with general psychological distress when they were examined individually. But they were risk factors in combinations with low social support at work for general psychological distress.

In addition, the combined risk of low job control and low social support click here at work were greater than the sum of their individual risks in both male and female workers. On the other hand, this study raises a question about the robustness of contemporary job stress models such as the DR and DCS models in which the possibility of synergistic interactions between resources or between job control and social support at work is selleck products not considered. Ignoring such interactions could result in limited validity of such models in reality (Schaubroeck and Fink 1998). For example, the DC and DCS models were only partially supported in this study (see the last FHPI molecular weight column of Table 5). The DC model (i.e., the highest risk in the low control and high job demand group) was supported in male workers only when social support at work was high (not when it was low) and in female

workers only when social support at work was low (not when it was high). The DCS model (i.e., the highest risk in the group of low control, high job demand, and low social support) was supported only in female workers (not in male workers). Therefore, in accordance with the position of Kasl (1996) and Schaubroeck and Fink (1998), it would be desirable to examine and report all possible interactions between job control, job demands, and social support at work on mental disorders beyond the DCS model-prescribed interactions between job control and job demands and between job strain and social support at work, particularly when the primary goal of a research is to test the DC and DCS models. Such practice will be useful for testing and advancing the models in the future because it could provide richer information about check when and why the models

do or do not work in reality. Also, this study has implications for psychosocial interventions to improve workers’ mental health in an economic downturn. It suggests that a substantial deterioration of workers’ mental health could be prevented by promoting either workers’ task-level control or workers’ internal solidarity or both (not necessarily both in women), even when the level of job demand is high. The management needs to adopt an internal work organization policy of empowering workers rather than depowering workers in an economic crisis for both workers’ mental health and productivity (Appelbaum and Donia 2000). Limitations of this study This study as a cross-sectional, secondary analysis study has a limitation for withdrawing a strong causal inference about the synergistic interaction effect between job control and social support at work on common mental disorders.

These instances of L-form induction and recovery closely mirror what we observe in Clostridium thermocellum. The destruction of the cell wall, or the failure to maintain it, may be representative of a cell struggling to keep or obtain the energy needed for survival. Once we determined that C. thermocellum L-forms were viable, we questioned why the cells would form an L-form rather than remain rod-shaped or form a spore. It seemed unlikely that L-forms Apoptosis inhibitor were deformed or unformed spores, as defects in spore formation manifest in identifiable stages, none of which resemble the L-form. We therefore hypothesized

that L-form formation provided some advantage for C. thermocellum. One potential explanation is that transitioning to an L-form requires less energy than sporulation or conserves energy overall for the cell. It is also possible that L-forms provide some advantage over spores or rod-shaped cells in terms of survival or recovery. Testing the first scenario effectively would have been technically difficult, so we went about testing the second hypothesis. To compare spores, rod-shaped cells, and L-forms in terms of survivability and recovery, we tested how well each cell type tolerated heat

and how quickly each could resume growth. C. thermocellum spores proved to be much better at tolerating heat stress than L-forms or rod-shaped cells suggesting advantages for C. thermocellum spores in prolonged survival under other stressful conditions.

L-forms did not survive heat stress as well as spores, but did exhibit a shorter lag-phase upon recovery when compared with both spores learn more and stationary phase cells, each of which took MEK inhibitor over 9 hours EPZ5676 molecular weight longer to begin exponential growth. While L-forms demonstrated faster recovery, L-form viability over time was consistent with that of stationary phase cells when subjected to prolonged starvation. This suggests that the primary advantage for C. thermocellum in forming an L-form does not lie in enhanced viability over time, but rather in the ability to recover rapidly when conditions become favorable for growth. This feature may allow for L-from cells to out-compete other non-growing cells in natural environments.What molecular or physiological triggers come into play to determine whether a cell becomes spore, an L-form or remain rod shaped remain to be explored. Conclusions In this work we were able to define conditions that gave rise to either spores or L-forms in C. thermocellum ATCC 27405. Of particular interest is the formation of spores in response to changes in substrate. This result suggests that C. thermocellum has a preference for continued cultivation on one substrate and variations in substrate supplied during cultivation may need to be minimized in order to optimize growth. To our knowledge this is the first documentation of the L-form state in C. thermocellum, and the first comparison between spores and L-forms in one organism.

Recently, Silvie et al. have described the MT81w mAb, which specifically recognizes mouse

CD81 Vistusertib chemical structure associated with other tetraspanins. This is evidenced by the lack of recognition of CD81 after cell lysis with detergents that do not preserve tetraspanin-tetraspanin interactions, and by the complete removal of the CD81 pool recognized by MT81w following immunodepletion of tetraspanin complexes [23]. CD81 is required for invasion of hepatocytes by sporozoites of human malaria Plasmodium falciparum and rodent malaria Plasmodium yoelii parasites [26]. Using MT81w antibody, Silvie et al. have shown that the subset of CD81 associated with TEMs contributes to Plasmodium sporozoite Ricolinostat purchase infection [23]. Such an antibody preferentially recognizing human CD81 associated with TEMs is not available. However, since Huh-7w7/mCD81 cells are susceptible to HCVcc and HCVpp-2a infection, we next took advantage of this model and the MT81w mAb to study the role of TEM-associated CD81 in the early steps of HCV life cycle. Using the MT81w anti-mCD81 mAb, we first characterized the subpopulation of mCD81 that is associated with TEMs on the cell surface of Huh-7w7/mCD81 cells (Figure 3A). As shown by flow cytometry

analysis, the intensity of MT81w labeling only reached 32 ± 14%, depending on the experiment, of the intensity with MT81 in Huh-7w7/mCD81 cells, indicating that only a fraction of CD81 molecules is engaged in tetraspanin microdomains on these cells, as described for Hepa1–6 cells [23]. However, we cannot exclude that the lower affinity of MT81w may lead to an underestimate this website of the ratio of CD81 engaged in TEMs. The specificity of MT81w to recognize TEM-associated CD81 in Huh-7w7/mCD81 cells was confirmed by immunoprecipitation experiments from biotinylated

cell lysates made under different detergent conditions. Tetraspanin microdomains Tau-protein kinase are typically disrupted by Triton X-100, but are retained in less hydrophobic detergents such as Brij 97 [30]. As shown in Figure 3B, 5A6 and MT81 mAbs precipitated hCD81 and mCD81, respectively, under both detergent condition. In contrast, MT81w was able to precipitate mCD81 only from Brij97 lysates preserving tetraspanin-tetraspanin interactions, but not from Triton X-100 lysates. These results show that expression of mCD81 in Huh-7w7 cells allowed to reconstitute tetraspanin webs that are specifically recognized by the well characterized MT81w mAb [23]. Figure 3 Recognition of TEM-associated CD81 in Huh-7w7/mCD81 cells. A, Flow cytometry analysis of Huh-7w7/mCD81 cells stained with the mAbs MT81 and MT81w. Cells stained only with PE-conjugated secondary antibody were used as control (dotted line). B, Cell lines were surface biotinylated and lysed in the presence of Brij97 or Triton X-100 before immunoprecipitation with MT81, MT81w and 5A6 mAbs. Immunoprecipitates were revealed by western blotting using peroxidase-conjugated streptavidin.

This is because the sides of cylinder and capsule nanorods are round but the side of rectangular nanorod is flat. Figure 3 Lifetime orientation GSK2118436 chemical structure distributions of QEs around (a, d) rectangular, (b, e) cylinder, and (c, f) capsule

gold and Si nanorods. The gold nanorods have wavelengths (a) 1,013, (b) 997, and (c) 946 nm, respectively. Four typical points are chosen: A (-70,0,0), B (-70,-10,0), C (-60,-20,0), and D (0,-20,0) nm. The lifetime orientation distributions of QEs around the rectangular, cylinder, capsule Si nanorods at wavelengths (d) 1,013, (e) 997, (f) 946 nm, respectively. As written in the Methods part, we define the anisotropy factor η to evaluate the orientation anisotropy by the ratio of the maximum lifetime over the minimum lifetime in all dipole orientations. The results of rectangular, cylinder, and capsule nanorods are shown in Table 1. The lifetime differs hundreds of times around the end of the rectangular nanorod. The orientation

anisotropy of the cylinder nanorod is much stronger than that of the rectangular nanorod. The orientation anisotropy of the capsule nanorod is the strongest, Bucladesine datasheet and the anisotropy factor reaches up to three orders of magnitude when the emitter is placed 10 nm to the end of the capsule nanorod. Table 1 Anisotropy factor η at different positions around gold nanorod   A B C D Rectangular 206 386 361 60.1 Cylinder 615 858 749 126 Capsule 1,016 837 794 137 In order to underline the effect of the localized surface plasmon, we consider dielectric nanorods with the same geometrical parameters but without plasmonic modes.

The material of the dielectric nanorod is chosen as Si with refractive index of 3.4. The orientation distributions around the rectangular, cylinder, and capsule dielectric nanorods at wavelengths 1,013, 997, Evodiamine and 946 nm are shown in Figure 3d,e,f, respectively. The green area is the cross Entinostat supplier section of the Si nanorod at z = 0 plane. We select the four typical points as before. We observe that the maximum of the color bar can be larger than 1. So in some dipole directions, the lifetimes of QEs will be longer than those of the vacuum. They are different from the lifetimes of the QE around the metallic nanorod. The anisotropy factors of the rectangular, cylinder and capsule-shaped dielectric nanorod are shown in Table 2. The lifetime differs only several times. The lifetime orientation anisotropy factors are much smaller than the metallic nanorod case. Table 2 Anisotropy factor η at different positions around Si nanorod   A B C D Rectangular 4.18 3.47 3.02 1.87 Cylinder 3.78 2.94 2.53 1.78 Capsule 2.96 2.30 2.21 1.85 In the following, we further study the detailed lifetime orientation distributions of the QE near the end of the capsule gold nanorod.

Our

experiment aimed to identify which drug-resistant OSI-027 price cell line is the ideal model for the study of the mechanism of hepatoma selleck drug-resistance and paves a way for the further investigation of drug-resistant and its reversal. Comparisons of three drug-resistance models The induction of multi-drug resistance in tumor cells was caused by factors such as P-gp [9], MRP, LRP, GST, glutathione, glutathione S-transferase, protein kinase C, apoptosis-related gene (bcl-2, c-myc, p53), and the high-expression of GCS in the cancer cell living environment and variation of DNA type II topoisomerase activity [10–17]. As the drug-resistant mechanism of tumors is quite complicated, the drug-resistant phenotype of MDR cells was contained in cell specificity, distinct inductive medicines and diverse induction methods, the concluded drug-resistant phenotype was not quite uniform [18–20]. In our experiment, we compared three types Epoxomicin molecular weight of multi-drug resistant human

hepatocellular carcinoma cell sub-lines ADM model established by three methods. The summary is shown below. Comparisons of biological characteristics in the three models The morphology of each drug-resistant cell line was irregular, volume was slightly increased compared with the parental generation, growth velocity was slower which enables accumulative growth, cell boundaries were obscure, massive particles and vacuoles were observed in the cytoplasm, and a slight shrinkage of the nucleus appeared. The in vitro induction of drug-resistant cells showed significant differences and the morphology of drug-resistant cell induced by in vivo implantation was close to the parental generation. The doubling times of the three drug-resistant cell lines, which were significantly extended compared with the parent cell line, revealed that growth velocity and the reproductive activity of the

drug-resistant cell line applied by an in vitro concentration gradient incremental method was significantly lower than that of the other two kinds of in vivo inductions. For the mechanisms of drug-resistance, the higher increase of drug excretion induced by a drug efflux pump was one of the most common drug-resistant reactions [21]. For this reason, we detected and compared the influx and efflux of ADM in three kinds of cells. Alanine-glyoxylate transaminase The results indicated that the efflux rates of the four groups were 34.14%, 61.56%, 66.56% and 81.06%. Efflux rate of ADM by the resistant cell was significantly increased which was reflected as the drug stagnation diminished. This caused the intracellular drug concentration to decrease and diminish the impairment of cell target organs by drugs, which is presumed to be the main cause of the higher drug-resistant index. Expressions of P-gp and MRP in the three groups of drug-resistant cells were significantly increased compared with the parental generation. The expression of GSH/GST in the three groups showed no statistical significance by paired comparison (P > 0.05).

4 994 57.8 selleckchem Fatigue 3 0.3 10 0.6 Headache 1 0.1 3 0.2 Temperature > 38°C 3 0.3 9 0.5 Myalgia 33 2.9 119 6.9 Lymph node swelling 1 0.1 –   Mild local reaction 141 12.3 654 38.0 Strong local reaction 8 0.7 32 1.9 Total 1,144 100.0 1,720 100.0 * Multiple responses were possible Between 26 October 2009 and 2 March 2010, 245 HCWs with ILS (4.4%) were referred to the pH1N1 task force in the Emergency Department (Table 1). The peak in ILS and pH1N1 infection in HCWs came in the 49th week of 2009. ILS occurred less often in pH1N1-vaccinated HCWs (OR 0.7; 95% CI 0.51–0.95), while the seasonal TIV showed no protective effect against ILS (OR 1.0; 95% CI 0.79–1.36). Gender was not associated with ILS (Table 4). Younger workers were more likely to present with ILS (OR for ≤30 years: 2.7; 95% CI 1.69–4.42). After adjusting for vaccination, nurses (OR 2.5; 95% CI 1.53–4.09) and physicians (OR 2.0; 95% CI 1.21–3.41) had a higher risk of developing ILS than administrators.

Table 4 Logistic regression for putative risk factors of influenza-like symptoms (ILS) Variable ILS OR 95% CI Neg. Pos. N (%) N (%) pH1N1 vaccination  No 3,690 (95.3) 182 (4.7) 1 –  Yes 1,657 (96.3) 63 (3.7) 0.7 0.51–0.95 Seasonal TIV 09/10  No 2,658 (95.9) 115 (4.1) 1 –  Yes 2,689 (95.4) 130 (4.6) 1.0 0.79–1.36 Gender          Female 3,856 (95.4) 186 (4.6) 1 –  Male 1,491 Dibutyryl-cAMP research buy (96.2) 59 (3.8) 0.9 0.64–1.18 Age (years)  ≤30 1,379 (93.7) 92 (6.3) 2.7 1.69–4.42  31–40 1,638 (95.0) 86 (5.0) 2.3 1.42–3.72  41–50 1,191 (96.4) 45 (3.6) 1.8 1.01–3.03  >50 1,139 (98.1) 22 (1.9) 1 – Profession  Nurses 1,854 (93.5) 128 (6.5) 2.5 1.53–4.09  Physicians 1,330 (95.5) 63 (4.5) 2.0 1.21–3.41  Auxiliary staff 1,239 (97.3) 34 (2.7) 1.1 0.63–1.95  Administration or others 924 (97.9) 20 (2.1) 1 – Out of the 97 pH1N1 infections, 91 (94%) occurred in

non-vaccinated HCWs and two (2%) in 4-Aminobutyrate aminotransferase HCWs vaccinated less than a week before the onset of symptoms. Overall, pH1N1 incidence was 1.7% of all HCWs, affecting 0.3% of those vaccinated and 2.4% of those not vaccinated (Table 5). The seasonal TIV did not protect against pH1N1 infection (OR 1.5; 95% CI 0.98–2.27) and neither did consecutive seasonal TIV in 2008 and 2009 (Table 1) (data not shown). Young HCWs were more often affected (OR for ≤30 years: 6.6; 95% CI 2.57–16.8, Table 5). A total of 41 pH1N1 click here infections would have been expected in the vaccinated HCWs if they had not been vaccinated.