, 2012) The findings

presented above may reassure parent

, 2012). The findings

presented above may reassure parents and providers who are reluctant to vaccinate due to concerns about risk compensation. However, as noted by Stupiansky and Zimet (2013), “… it is important to remember that risk compensation (real or imagined) is find more not a rationale for withholding vaccine. Instead, it is a rationale for ensuring adequate education both pre- and post-vaccination” (p. 262). Underlying some parental HPV vaccine concerns (e.g., feeling that HPV vaccine is too new) are questions about vaccine safety (Fisher, 2012; Krawczyk et al., unpublished results). Fear-inducing news stories may have contributed to these concerns as they sometimes have misreported Vaccine Adverse Event Reporting System data, incorrectly suggesting that HPV vaccination has often led to severe adverse health effects, including death (see, for example the August, 2007 edition of Maclean’s magazine in Canada; Gulli, 2007). Numerous large-scale studies on HPV vaccine safety have been published and show little or no evidence of severe side-effects associated with vaccination

(Agorastos et al., 2009, Chao et al., 2012, Gee et al., 2011, Klein et al., 2012 and Lu et al., 2011). HA-1077 The most frequently reported side-effects are similar to those reported with other vaccines and are transient events, such as mild pain and bruising at the injection site, faintness, and syncope (Naleway et al., 2012). It is important to highlight that a reported adverse event after vaccination does not automatically mean that it was caused by the vaccine. A major challenge, however, is how to effectively communicate to parents the evidence that HPV vaccine is quite safe. As noted following, an additional challenge involves communicating Fossariinae the very substantial risks of non-vaccination, in the context of generalized, relatively early, sexual debut, delayed marriage, serial monogamy, and the accumulation of risk of HPV infection over

time. Development of effective strategies for clearly and accurately communicating information about risk of vaccines has been an enduring focus of vaccine researchers (Ball et al., 1998, Betsch and Sachse, 2013, Davis et al., 2001 and Offit and Coffin, 2003). Best practices in this regard may rest on the nature of the vaccine (routine versus elective), the controversies that may surround the vaccine (e.g., MMR and autism, HPV and risk compensation), and, importantly, whether parents or patients harbor ongoing concerns about HPV vaccine safety, actively ask about vaccine safety, or have no concerns in this area. Suggestions for communication about HPV vaccine safety include asking patients whether they have any questions about the vaccine and providing accurate information (including credible websites) that can address concerns about safety.

Based on this data, a cut-off of ≥75% can be defined to suggest B

Based on this data, a cut-off of ≥75% can be defined to suggest BTV replication and to identify animals in which the virus can replicate sufficiently to transmit, as soon as 2–3 weeks after infection. This

cut-off would probably be lower under field conditions. Our results indicate that SubV is potentially DIVA compliant under these conditions but would need to be validated with samples from naturally infected animals. In conclusion, an experimental BTV vaccine consisting of VP2, NS1, and NS2 induced diverse immune response and is a promising candidate vaccine that provides strong clinical and virological protection against experimental BTV-8 infection in cattle. Further investigations of SubV should be performed, including exchanging or combining VP2 of other serotypes to test the vaccine’s adaptable nature and evaluating the duration of immunity. The FG-4592 molecular weight DIVA compliancy of this vaccine should also be evaluated under field conditions. This work was supported by the Swedish Research Council Formas (grant 2009-1593). The research leading to these results has also received funding from the European Community’s Seventh Framework Programme (FP7, 2007-2013), Research Infrastructures action, under the grant agreement No. FP7-228394 (NADIR project, coordinated by F. Lantier, INRA, France). http://www.selleckchem.com/products/PLX-4032.html We thank Karin Selin-Wretling and Annika Rikberg at the Swedish University of Agricultural

Sciences as well as the staff at the Department of Virology, Immunobiology, and Parasitology at the Swedish about National Veterinary Institute for help with assays. We also thank Pierre Sarradin as well as Céline Barc and the PFIE technical staff. “
“One of the largest impediments to efficient immunization is the wastage of opened and unopened vaccine vials [1]. As developing countries introduce new and expensive vaccines, there is a need to understand factors that contribute to vaccine wastage so potential solutions can be assessed. Vaccine wastage is defined by the World Health Organization (WHO) [2] as “loss by use, decay, erosion, or leakage or through wastefulness”, and can be calculated

as the proportion of vaccine administered against vaccine issued [1]. Vaccine wastage falls into two categories: wastage in unopened vials and wastage in opened vials. Wastage in unopened vials results from expiration, thermo-instability, breakage, missing inventory, and other incidental causes [3], and is generally a static rate [4]. Wastage in opened vials is much higher than in unopened vials [5], and varies from facility to facility. It is related to many factors including immersion of opened vials in water, uncertainty about the sterility of prior withdrawals, thermal handling, and poor vaccine administration practices [1]. With the use of a multi-dose vial (MDV), there is a risk of contamination every time a needle is inserted into the vial.

Clinical trials of RV1

in Latin America found high effica

Clinical trials of RV1

in Latin America found high efficacy (91%; 95% CI: 71–98%) against severe (Vesikari score ≥11) rotavirus gastroenteritis due to G1P [8] but lower, non-significant efficacy (45%; 95% CI: −82 to 86%) against G2P [4] and [1]. However, a subsequent trial in Europe with a larger sample size showed high levels of protection against severe rotavirus gastroenteritis due to G1 (96%; 95% CI: 90–99%) and G2 strains (86%; 95% CI: 24–99%) as well as G3 (94%; 95% CI: 53–100%), G4 (95%; 95% CI: 68–100%), and G9 strains (85%; 95% CI: 72–93%) [8]. The RV1 clinical trials in Africa showed similar efficacy against G1 strains (64%; 95% CI: 30–82%) and non-G1 strains (60%; 95% CI: 37–74%) [18]. The clinical trial of RV5 in the USA and Finland observed a 95% (95% CI: 92–97%) rate reduction in the number of hospitalizations selleck kinase inhibitor and emergency department visits due to G1 strains and rate reductions of 93% (95% CI: 49–99%), 89% (95% CI: 52–98%), and 100% (95% CI: 67–100%) in the number of hospitalizations and emergency department selleck products visits due to G3, G4, and G9 strains, respectively [2]. The RV5 clinical trial in Africa provided significant protection against severe gastroenteritis due to G8 strains (88%; 95% CI: 7–100%),

P1A[8] strains (36%; 95% CI: 4–58%), and P2A[6] strains (48%; 95% CI: 10–70%) [21]. In the RV5 clinical trial in Asia, strain-specific vaccine efficacy estimates were imprecise due to small numbers and the trial observed significant protection only against P1A[8] strains (50%; 95% CI: 19–69%) [22]. Strain-specific vaccine efficacy estimates from the clinical trials are limited to the predominately circulating strains at the time of the trials. However, post-licensure vaccine effectiveness data from countries that have introduced rotavirus vaccine Idoxuridine into their routine immunization programs have enabled vaccine performance against a variety

of strains in a variety of settings to be evaluated. Of particular interest has been the apparent emergence of G2P[4] in Brazil and Australia following the introduction of RV1 in these countries [52] and [53]. G2P[4] is fully heterotypic compared to the RV1 strain and there was some concern that the selective pressure of the vaccine may have led to its predominance. However, vaccine effectiveness studies in Brazil found that RV1 was 39–89% effective against severe disease caused by G2P[4] strains although the effectiveness may wane in children >12 months of age [36], [54] and [55]. RV1 was 83–85% effective against rotavirus gastroenteritis due to G2P[4] in children 6–11 months of age in Brazil but only 5–41% effective in children ≥12 months of age [54].

Treatment consisted of DMSO, C-DIM-5 (10 μM, 20 μM), C-DIM-8 (10 

Treatment consisted of DMSO, C-DIM-5 (10 μM, 20 μM), C-DIM-8 (10 μM, 20 μM), doc (10 nM), C-DIM-5 (10 μM, 20 μM) + doc (5 nM), and C-DIM-8 (10 μM, 20 μM) + doc (5 nM). After 48 h cells were washed twice with PBS, permeabilized with 100 μl pre-chilled PBS and stained with 8 μl of staining solution (i.e. ethidium bromide [100 μg/ml] + acridine orange [100 μg/ml] in PBS). The cells were viewed under an Olympus BX40 fluorescence microscope connected

to a DP71 camera (Olympus, Japan). Apoptotic cells were quantified and the results presented as means of percentage apoptotic cells ± SD normalized against control. The in vitro efficacies of the aerosolized C-DIM formulations were evaluated in A549 cells using a six-stage viable impactor connected to the Pari LC Star jet nebulizer and operated for 5 min at a flow rate of 28.3 l/min. A549 cells (106 cells Protein Tyrosine Kinase inhibitor in 15 ml of medium) were seeded check details in sterile petri dishes (Graseby Andersen, Smyrna, GA) and placed on stage 1 through stage 6 of the viable impactor. A549 cells were exposed to nebulized C-DIM-5 and C-DIM-8 for 2 min. The petri dishes were then incubated at 37 °C for 72 h under aseptic conditions. Untreated cells

were used as a control. Cells were washed with PBS and detached from the petri dish using trypsin. Cells were pelleted by centrifugation at 5000g for 5 min and resuspended in media. Cell viability old was determined by the trypan blue method ( Zhang et al., 2011). Fluorescence activated cell sorting (FACS) analysis of cell cycle dynamics was carried out as previously described (Li et al., 2012). A549 cells (104 cells/well) suspended in F12K growth media were seeded in a 96-well plate format. Treatment consisted of DMSO, C-DIM-5 (10 μM, 20 μM), or C-DIM-8 (10 μM, 20 μM)

and incubation at 37 °C for 24 h. Cells were harvested using 0.25% trypsin and centrifuged for 5 min at 5000g. Cells were washed in 5 ml of PBS containing 0.1% glucose. Cells were then resuspended in 200 μl of PBS, followed by permeabilization and fixation by drop wise addition of 5 ml pre-chilled ethanol (70%) and kept at 4 °C for 1 h. Cells were pelleted and washed with 10 ml PBS. The cell suspension was incubated in 300 μl staining solution comprising of 1 mg/ml propidium iodide (PI) and 10 mg/ml RNAse A (Sigma Aldrich, St. Louis, MO). Cells were incubated at 37 °C for 1 h and analyzed by FACS using the BD FACSCALIBUR. CaCo2 cells were grown in DMEM media fortified with 10% fetal bovine serum, 1% non-essential amino acids, 10 mM HEPES, and a penicillin/streptomycin/neomycin cocktail in 75 cc flasks. Cells were maintained under conditions of 5% CO2 and 95% humidity at 37 °C. Sub-cofluent CaCO2 monolayers were washed with Dulbecco’s phosphate-buffred saline (DPBS) 2× and detached with trypsin-EDTA (0.25%) and seeded (5.0 × 104) in a 0.5 ml-volume into the apical chamber (with 1.

Regardless, there is clearly a need for targeted therapies for Ge

Regardless, there is clearly a need for targeted therapies for GemA that can delay or prevent progression UMI-77 ic50 to GBM. However, until now there has been no useful animal model of GemA available to test adjuvant therapy after surgical debulking as humans are treated. Furthermore, the murine models of glioma have not been predictive of toxicity or

efficacy in humans, and this has undoubtedly contributed to the painstakingly slow progress in therapeutic development. Similarly to humans, dogs develop spontaneous brain tumors that often carry a dismal prognosis. Based on an incidence of primary brain tumors in dogs of 20 per 100,000/year, it has been estimated that 12,000 dogs could be eligible for recruitment into clinical studies in the United States annually [5]. We and others have found many similarities between human and canine glioma such as: overexpression of the epidermal growth factor receptor, mutation of the Tp53 tumor suppressor gene [6], extensive invasion into normal brain, peritumoral edema and necrosis [7] and [8], hemorrhage, compression, herniation, and obstructive hydrocephalus Selleckchem Enzalutamide [9], [10] and [11]. Similar to humans, the prognosis for dogs with brain tumors is poor regardless of therapeutic intervention. However, much less is known about treatment outcomes

because of a historical lack of treatment options in dogs and because only a small number of studies, each of which includes few dogs, have been reported. The median survival time for dogs with glioma (any grade) that do not receive any type of treatment ranges between 6 and 13 days [9] and [10]. In dogs receiving only palliative

therapy the range is 60–80 days [12] and [13]. Radiation therapy may have resulted in an increased survival time in one dog with glioma (176 days) as mafosfamide compared to corticosteroid therapy in three dogs with glioma (18, 40 and 64 days) [12]. The median survival for 9 dogs putatively diagnosed with glioma at our institution based on imaging characteristics of an intra-axial mass was 29 days (range 1–128 days). These dogs did not receive any therapy other than corticosteroids and anticonvulsants. The clinical similarities between dogs and humans suggest that dogs may represent an outstanding model for testing targeted therapies; both dogs and humans might benefit from these studies. We previously developed a dendritic cell culture-free vaccine consisting of glioma cell lysate and CpG ODN, “CpG/Lysate”, that significantly extended survival of glioma-bearing mice [14]. CpG ODN is a potent vaccine adjuvant that signals through toll like receptor nine (TLR9) in dendritic cells and B cells to induce adaptive anti-tumor immune response in murine models and select cancer patients (reviewed in [15]).

While the bicycle is increasingly used for sport and recreation a

While the bicycle is increasingly used for sport and recreation activity, just over one-fifth of adults reported engaging

in either road cycling or mountain biking at least once over twelve months in the most recent national www.selleckchem.com/products/Dasatinib.html survey (Sport New Zealand, 2009). For many people, safety concerns are a major barrier to riding a bicycle (Kingham et al., 2009, Mackie, 2009 and Winters et al., 2011) and it is true that cyclists bear a higher risk than most other types of road users if time-based exposure is considered (Tin Tin et al., 2010 and Wardlaw, 2002). For each million hours spent cycling on New Zealand roads, 29 deaths or injuries resulted from collisions with a motor vehicle (cf. 10 car driver deaths/injuries, 7 car passenger deaths/injuries and 5 pedestrian deaths/injuries) (Ministry of Transport, 2012b) and 31 injuries resulted in death or hospital inpatient Z-VAD-FMK price treatment (cf. 2 driver injuries, 3

car passenger injuries and 2 pedestrian injuries) (Tin Tin et al., 2010). Furthermore, almost as many bicycle crashes occurred off-road (Munster et al., 2001). Current statistics and epidemiological research in New Zealand and elsewhere (Amoros et al., 2011, Beck et al., 2007, Boufous et al., 2012, Buehler and Pucher, 2012, Garrard et al., 2010, Ministry of Transport, 2012b and Tin Tin et al., 2010) typically refer to a single official data source, either police reports or hospital records, which are known to undercount bicycle crashes (Elvik and Mysen, 1999, Langley et al., 2003 and Tercero and Andersson, 2004). Other studies

have relied on cross-sectional survey data (Aultman-Hall and Kaltenecker, 1999, Heesch et al., 2011 and Moritz, 1997) thereby failing to account for reverse causation and potential biases (af Wåhlberg et al., 2010, Jenkins et al., 2002 and Tivesten et al., 2012). Few prospective studies have reported the incidence and correlates of bicycle crash injuries (de Geus et al., 2012 and Hoffman et al., 2010) but not the findings could have been biased by differential loss to follow-up (Greenland, 1977). This paper investigated the incidence of attended bicycle crashes and associated factors in a cohort of cyclists followed over a median period of 4.6 years. Attended bicycle crashes include those resulting in an admission to hospital, notification to the police or the Coroner (Medical Examiner), or a claim lodged with the Accident Compensation Corporation (ACC), the government-funded universal no-fault injury compensation scheme. The Taupo Bicycle Study is a prospective cohort study with the sampling frame comprising cyclists, aged 16 years and over, who enrolled online in the Lake Taupo Cycle Challenge, New Zealand’s largest mass cycling event held each November. Participants have varying degrees of cycling experience ranging from competitive sports cyclists to relative novices of all ages. Recruitment was undertaken at the time of the 2006 event.

009 μg/μl, resulting in the absence of visible DNA bands on the g

009 μg/μl, resulting in the absence of visible DNA bands on the gel. Most likely, the integrity of the pDNA in lPEI polyplexes was affected during nebulisation. Nebulisation of brPEI polyplexes seemed to have no effect on their stability as no DNA fragment was visible in lane 9. In addition, it is very likely that the DNA integrity in the brPEI polyplexes was not affected during nebulisation, because a small DNA fragment without a smear is visible in lane 10. To verify this, we determined the gene expression Volasertib of brPEI polyplexes before and after nebulisation. As an extra control, the gene expression of lPEI polyplexes was also verified. As shown above (Section 3.4), non-nebulised lPEI complexes transfected twice

as much BGM cells as brPEI complexes (Fig. 2B and C). However, nebulised lPEI complexes

were no longer able to transfect BGM cells, whereas the transfection capacity of brPEI complexes was not affected by nebulisation, except Bioactive Compound Library purchase when using 1.26 μg DNA. These results confirm the observed destabilisation of lPEI complexes following nebulisation. Based on these data we selected the brPEI polyplexes (with N/P 8) for further in vivo vaccination experiments in turkeys. Turkeys were vaccinated and challenged following the protocols described in material and methods and summarized in Table 1 and Table 2. During these vaccination experiments we followed up clinical signs, examined the presence of macroscopic lesions, the presence of Cp. psittaci in tissues and excretions, and the immune response. Clinical signs were first observed for the non-vaccinated control group (group 4), 5 days PC. At that time, 4 of 7 (57%) turkeys showed conjunctivitis and clinical disease gradually increased. Severe clinical disease, characterised by conjunctivitis, rhinitis, dyspnoea and watery droppings was only observed in controls, especially from day 11 PC until day 18 PC, being most severe at 13 almost and 14 days PC when all 7 control animals showed severe clinical disease. From day 19 until day 22 PC, only conjunctivitis (5 of 7; 71%), rhinitis (3 of 7; 43%) and watery droppings (2 of 7; 29%) could be observed. From day 23 PC onwards, only conjunctivitis (5

of 7; 71%), rhinitis (3 of 7; 43%) and moderate dyspnoea (2 of 7; 29%) was present. Dyspnoea and watery droppings were not observed in the vaccinated groups (groups 1–3). Conjunctivitis and rhinitis where the only clinical signs noted and were observed for all animals of group 1 (day 9 until day 11 PC), group 2 (day 7 until day 9 PC) and group 3 (day 7 until day 13 PC). Based on the clinical signs, best protection occurred for group 2 followed by groups 1 and 3. At euthanasia, all turkeys were examined for macroscopic lesions (Suppl. Table 1A). All non-vaccinated turkeys (group 4) showed diffuse opacity of the airsacs with multiple large fibrin deposits, especially in the abdominal airsacs. Sero-fibrinous pericarditis was present in 3 of 7 (43%) of all control animals.

Some published trials have identified a shorter weaning period af

Some published trials have identified a shorter weaning period after inspiratory muscle training (Cader et al 2010, Cader et al 2012), while Caruso et al (2005) and our study did not. The study by Caruso et al failed to achieve a significant improvement in

inspiratory muscle strength from their inspiratory muscle training, and this may explain why weaning duration was unaffected. However, given the relatively large improvement in inspiratory muscle strength in our study, it is unclear why this did not carry over into improvement in weaning duration. Also, our study had a much larger sample size than these other studies, although it did not quite achieve the calculated sample size due to slightly greater loss Autophagy inhibitor concentration to follow-up than anticipated. Therefore, differences in the study populations and perhaps a slight lack of statistical power may each have contributed to the lack of an effect on weaning duration in our study. Although the training did not impose a load on the expiratory muscles, a significant effect on maximal expiratory pressure was observed. This counterintuitive result may be a chance finding. However,

the intercostal muscles may contribute to both inspiratory and expiratory efforts (De Troyer et al 2005). Therefore it is possible that these muscles may contribute to the improvement in maximal expiratory pressure. If this finding represents Cyclopamine mw a true effect, it may be a valuable one. The contraction of expiratory muscles

is one of the three events in the production of cough (Pitts et al 2009). Cough strength may be an important predictor of weaning, with patients who have weak or no cough being more likely to have unsuccessful extubations than those with clearly audible, moderate or stronger coughs on command (Khamiees et al 2001). Unfortunately, none of the other randomised trials in this area measured maximal expiratory pressure (Caruso et al 2005, Cader et al 2010, Cader et al 2012, Martin et al 2011). In our study, tidal volume showed a significant increase in the intervention group compared to the control group. Adequate tidal volume is an important predictor of weaning success, since the rapid shallow breathing index tends to be higher in patients who fail extubation, and this can be due to increased Parvulin respiratory rate and/or decreased tidal volume (Segal et al 2010). Other randomised trials of inspiratory muscle training in patients receiving mechanical ventilation did not measure its effect on tidal volume. The rapid shallow breathing index was evaluated in our study and showed a decrease in both groups, although the within-group and between-group differences were all non-significant. In contrast the results reported by Cader and colleagues (2010) showed an increase (ie, worsened) in both groups over the weaning period, but the increase was attenuated significantly by the inspiratory muscle training.

The mixture was filtered using 0 22 μm milipore filter with vacuu

The mixture was filtered using 0.22 μm milipore filter with vacuum assistance and sonicated by ultrasonic bath for 15–20 min. A stock solution was prepared by dissolving accurately weighed 100 mg of clebopride in 100 mL of methanol to yield a final concentration of 1 mg/mL, sonicated for 5 min, allowed to equilibrate to room temperature. The stock solution (1000 μg/mL of clebopride) was diluted suitably and spiked with human blank plasma to get 1–60 ng/mL of drug. 200 μL of each calibration standards were pipetted http://www.selleckchem.com/products/PLX-4032.html into a series of Ria vial tube and vortexed briefly. 3 mL of mixture of diethyl ether: dichloromethane (50:50 (v/v)) was added to each

Ria vial and caped. All calibration samples were vortexed for approximately for 3 min and centrifuged at 4000 rpm for approximately 5 min at 10 °C. The organic layer (2.0 mL) was quantitatively transferred to a 4 mL glass tube and evaporated to dryness at 40 °C under a stream of nitrogen. Then, the dried extract was reconstituted Selleckchem Y 27632 in 200 μL of mobile phase and a 20 μL aliquot was injected into the chromatographic system using Hamilton syringe. The drug was estimated at 283 nm using UV detector to maximize the signal of compound and minimize the

signal of plasma interferents. The ratio of mobile phases was optimized by several trials to get good resolution and symmetric peak shape for the clebopride. The developed HPLC method was optimized by monitoring chromatographic parameters including retention time, column efficiency (HETP) of the various variations of composition, and flow rate of mobile phase. Efficiency values (N) showed the results of ≥4400, this suggested that the sharp peak produced enough. The system isothipendyl suitability parameters are given in Table 1. The developed method was evaluated for linearity, selectivity, accuracy and precision, stability during various stress conditions including bench top stability, freeze thaw stability, stability of stock solutions and dilution integrity and recovery. Blank plasma was tested for endogenous interference. Selectivity was evaluated by extracting different blank plasma samples. The

absence of interfering peaks at the same retention time of clebopride was considered as evidence for selectivity of the method. The typical chromatograms for the blank plasma and sample are given in Fig. 2 and Fig. 3 respectively. Calibration curve was plotted by taking concentration of analyte in X axis and detector response in Y axis. The developed method was linear in the concentration range of 1–60 ng/mL with the correlation coefficient value of 0.998. Slope and intercept of the linearity curve ( Fig. 4) was found to be 20.23 and 0.919 respectively. Recovery of clebopride was evaluated by comparing the detector response of clebopride in three quality control samples (LQC, MQC and HQC) with the response of same in equivalent methanolic solutions (Table 2).

In record speed, this facility was completed, certified cGMP-comp

In record speed, this facility was completed, certified cGMP-compliant and since June 2010 has been undergoing test operations within a validation programme. Much of the critical facility and process equipment has been procured and controlled for ZD1839 installation, operation, performance and maintenance qualification. The Master Validation Plan for influenza vaccine production was approved which contains the strategy for the validation of processes based on risk assessment, focusing primarily on sterility and viral safety. To increase production capacity to at least 1 million doses per year, IVAC installed hot and cold rooms in a dedicated space,

more incubator equipment and separate zones for in-process testing and the preparation of media and cleaning of equipment; inoculation and harvesting; and purification. Screening high throughput screening Independent technical units have been set up to serve as a contaminated area, a noncontaminated

area, and egg-handling and entrance, respectively. Each area is installed with separate heating, ventilation and air-conditioning (HVAC) systems. The HVAC systems and clean rooms have been qualified using a series of manufacturing runs, constant control of environmental conditions and digital direct controller system to stabilize room temperature, pressure and humidity. The quality control laboratory has been upgraded to meet international standards for influenza vaccine production and ancillary zones have been created for personnel. The waste treatment system

has been installed with high efficiency particulate air filters in outgoing airflows. Contaminated fluids from the production process are steam-sterilized before sending to the central fluid waste treatment station, and contaminated egg waste is kept in special bins for incineration after decontamination. A two-door autoclave for decontamination is in place, and a kill tank pressure vessel has been ordered, where liquids for decontamination will be collected and heated to 60–80 °C before disposal. Standard operating procedures have been prepared for the operation and maintenance of each piece of equipment. IVAC is implementing an environmental control programme for air quality which meets mafosfamide particulate and microbiological specifications. Systems to ensure purified water and water for injection will become fully operational in 2011 (see Table 1). Onset of the A(H1N1) influenza pandemic in 2009 switched the focus from (A)H5N1 to the novel pandemic strain. Eight initial batches of H1N1 influenza whole virion vaccine were produced at a scale of 7000 eggs and used to test and improve the performance of the production process equipment and enhance the skills of IVAC staff. The first batch was produced with assistance from the Netherlands Vaccine Institute (NVI) and all process steps were evaluated.