At predetermined time intervals the release medium was sampled (3 ml) and replaced with fresh pre-warmed dissolution media. Samples were diluted in PBS-T for concentration analysis by ELISA. For rods dissolution volume was 20 ml and sample volume was 2 ml. Dissolution volumes were selected to maintain sink

conditions. Stability assessment was carried out in a similar fashion to the described release EPZ-6438 research buy protocol. Following complete dissolution of the CN54gp140 containing lyophilized solid dosage tablets in PBS-T (30 ml) a sample was taken and diluted in PBS-T for concentration analysis by ELISA. Animals were assigned to experimental groups where n = 5 ( Table 1). Mice received a subcutaneous (s.c.) prime (Day 0) then an intra-vaginal (i.vag.) boost three times at 21-day intervals (Days 21, 42, 63) with vaginally administered rod formulations

( Table 1). Mice were lightly anesthetised and the rod formulations were inserted into the vagina using a positive displacement pipette (Gilson Microman – 100 μl maximum volume) and a tip with the end cut off and filed down to smoothness. To thin the vaginal epithelium and improve protein uptake, mice were treated subcutaneously with selleck kinase inhibitor 2 mg of depoprovera (in 50 μl PBS) 5 days prior to the first and third vaginal immunization. Blood samples were taken from the tail vein of mice on Days 20, 41, 62, and 83 and by cardiac puncture on Day 120. Blood samples were centrifuged following clotting for collection of sera. Vaginal lavages were PD184352 (CI-1040) conducted on Day 83. Vaginal lavages were collected and pooled by flushing the vaginal lumen three

times with a 25 μl volume of PBS using a positive displacement pipette. 5 μl of 25X protease inhibitor cocktail was added to the vaginal eluates, which were incubated on ice for 30 min prior to centrifugation to remove the mucus/cellular pellet. All samples were stored at −80 °C until analysis. Binding antibodies against CN54gp140 in vaginal lavage and serum samples were measured a quantitative ELISA. 96-Well plates were coated with CN54gp140 and blocked with 1% BSA as before. IgG or IgA standards were used on each plate to quantify the CN54gp140 specific antibodies. Experimental samples were diluted 1:100, 1:1000 and 1:10,000 (sera) or 1:10 and 1:50 (lavage) to ensure the absorbance reading measured fell within the linear range of the standard curve. Bound IgG was detected by incubation for 1 h at 37 °C with HRP-conjugated goat anti-mouse IgG, bound IgA was detected using biotinylated anti-mouse IgA and followed by Streptavidin-HRP. Plates were washed and developed with 50 μl TMB/E substrate and the reaction was terminated by the addition of 50 μl of 2 M H2SO4 and read at A450. Vaginal lavage values were normalised against the total IgA or IgG measured in the same sample. Semi-solids (Table 2) were prepared using either an overhead stirrer or HiVac® bowl, the choice of which was dependent upon the viscosity of the systems being prepared.

For feature-based magnitude coding, we calculated ARed – ABlue, where ARed and ABlue indicate the activity Bioactive Compound Library rates for trials when the red or blue stimuli, respectively, appeared farther from the reference point. Analogous differences were calculated for the duration task. In the matching task, we calculated only ARed – ABlue. Figure S4 presents normalized preference indices in the form of contrast ratios: (ARed – ABlue)/(ARed + ABlue) or (AS2 – AS1)/(AS2 + AS1). We also used population activity averages to assess the magnitude of coding. We designated the condition associated

with the highest discharge rate (e.g., S2 longer or farther) as the preferred condition and the one with the lowest activity as the antipreferred condition, and we calculated the population averages as the means of separately calculated single-cell averages, along with the SEM. Near the end of recording, we made electrolytic marking lesions (15 μA for 10 s). Ten days later, the monkeys were deeply anesthetized selleck chemicals and perfused with 10% formol saline. We plotted recording sites on coronal Nissl-stained sections, by reference to the recovered marking lesions, pins inserted during the perfusion, and structural magnetic resonance images. Although the entry points for more posterior recordings (Figure 1D) make it appear that many cells were located in the postarcuate cortex, track reconstructions based on the

angle and depth of penetrations indicated

that nearly all recordings in caudal PF came from Fossariinae the prearcuate cortex, which corresponds to area 8. This work was supported by the Division of Intramural Research of the NIMH (Z01MH-01092) and by Grants-in-Aid to S.T. from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) (23119714) and the Japanese Society for the Promotion of Science (JSPS) (22700340) in Japan. We thank Dr. Andrew Mitz, Mr. James Fellows, and Ms. Ping-yu Chen for technical support. “
“Loss of spinal cord dorsal horn inhibitory circuits, many of which involve interneurons that express gamma aminobutyric acid (GABA), is one of the major contributors to the persistent neuropathic pain that can follow nerve injury. The loss of inhibition contributes not only to the development of spontaneous pain but also to the hyperexcitability that underlies the mechanical hypersensitivity (allodynia) and exacerbated pain (hyperalgesia). For example, partial sciatic nerve injury reduces spinal GABA release and expression of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD; Moore et al., 2002). The consequence of this is a loss of inhibitory tone in the dorsal horn. It is not clear, however, whether the reduced GABAergic inhibition results from injury-induced degeneration of GABAergic interneurons (Scholz et al., 2005 and Sugimoto et al., 1990), reduced primary afferent input to these interneurons (Kohno et al.

Additionally, FomA has been recognized as a major immunogen of F. nucleatum [16] and [17]. Intriguingly, it has been reported that FomA is involved in binding between fusobacteria and Streptococcus sanguis on the tooth-surface and to Porphyromonas gingivalis (P. gingivalis)

in the periodontal pockets [18], supporting the view that FomA acts as a receptor protein in co-aggregation with other oral pathogenic bacteria. Thus, FomA is a potential target for the prevention of bacterial co-aggregation. Nutlin3a Classical treatments for periodontal diseases involve not only mechanical and antibiotic therapies but also surveillances on dynamic processes including the periodontopathogenic bacteria and the host responses. Chemical antiseptics are also used for treatments of periodontitis and halitosis. However, most of the chemical antiseptics fail to cure chronic, severe periodontitis and halitosis. Treatments using multiple doses of antibiotics to cure infection-induced periodontitis and halitosis have risks of generating resistant Ibrutinib nmr strains and misbalancing the resident

body flora [19]. In addition, even though bacteria in the dental biofilm can invade the periodontal tissues, most of bacteria located in the dental biofilm and outside the host tissues are inaccessible to antibiotics. The treatments of periodontitis and halitosis have not been significantly improved during the past 40 years due to the lack of focus on the awareness that these diseases are polymicrobial diseases as opposed to mono-infections. Vaccines targeting oral bacteria [such as Streptococcus mutans (S. mutans) for dental caries; P. gingivalis Resveratrol for periodontitis] are currently being evaluated [20] and [21]. However, these vaccines cannot combat the enhanced pathogenesis (e.g. co-aggregation/biofilms) by F. nucleatum. Since the plaque biofilm is a common feature for almost all oral

bacteria, blocking the bacterial co-aggregation at an early stage in biofilm formation will broadly prevent various biofilm-associated oral diseases including periodontitis and halitosis [22]. In the study, we demonstrate that F. nucleatum FomA is immunogenic, and that mice immunized with FomA produce neutralizing antibodies which prevent bacterial co-aggregation and, also gum abscesses and halitosis associated with co-aggregation. Moreover, immunization with FomA conferred a protective effect on bacteria-induced gum swelling and decreased the production of macrophage-inflammatory protein-2 (MIP-2) cytokine. These findings envision a novel infectious mechanism by which F. nucleatum interacts with P. gingivalis to aggravate oral infections. Moreover, this work has identified FomA as a potential molecular target for the development of drugs and vaccines against biofilm-associated oral diseases. F. nucleatum (ATCC® 10953) and P. gingivalis (ATCC® 33277) were cultured in 4% (w/v) trypticase soy broth (TSB, Sigma–Aldrich, St. Louis, MO) supplemented with 0.

To address open vial wastage, the WHO has a multi-dose vial policy Epigenetics Compound Library chemical structure (MDVP) that permits vials of certain vaccines to remain open for up to 4 weeks so long as certain criteria are met regarding handling, administration, and storage [7]. Some local health programs may

feel that they are unable to meet these conditions (for instance, in rural vaccination clinics or outreach settings) and workers may discard open vials after each clinic day. With certain vaccines, the MDVP may not apply [4] and [8]. For countries and clinic settings that cannot comply with the WHO MDVP, there are two driving factors that influence open vial vaccine wastage: (1) the session size of a vaccination facility, and (2) the vaccine vial size [8] and [9]. The larger the session size (the more children who showed up for vaccination during one session), the fewer the overall remaining doses. One strategy that has been examined to help reduce open vial wastage is to lower the number of doses per vaccine vial [2] and [3]. A 2012 study found that in primary care settings in urban India, vial size is statistically significantly related to vaccine wastage [10]. While switching to lower dose vials might reduce open vial vaccine wastage, it will incur higher purchasing, manufacturing, storage and vaccine delivery

costs. Moreover, many new vaccines come at a higher Stem Cell Compound Library datasheet price per dose than traditional vaccines, and thus wastage is more costly [11]. A 2009 study found that the optimal vial size depends on country-specific wastage rates, and concluded that these critical data are missing for most GAVI eligible countries [12]. In 2010, Lee et al. [6] applied a mathematical model to capture the vaccine wastage and associated economic impact of different vial size strategies. Due to the lack of facility data in real-life

settings, the paper assumed that session size follows a Poisson distribution. Rolziracetam The paper emphasized that in order to calculate the expected wastage rate, one needs to first define the distribution of session size. No studies have since collected data on vaccine session sizes and defined a statistical distribution to generate open vial vaccine wastage as an output. In our study, we used session size data from four countries to develop a realistic statistical model of open vial wastage rates and their associated costs. We use the term “session size” in our study to refer to the number of children who arrive at a given vaccination session. There were two primary objectives to this study: first, to use session size data from four GAVI-eligible countries to understand country-level factors that influence wastage in open vials; second, to estimate the economic impact of switching to smaller dose vials. The Strategic Advisory Group of Experts on Immunization (SAGE) recommended inactivated polio vaccine (IPV) to be introduced to the routine immunization program by 2015 [13].

A correction factor (0.91) was applied to the 3200 cpm (Puyau et al., 2002) threshold to yield a MVPA cutpoint of 2912 cpm (Corder et al., 2007). To limit participant burden, only maternal parenting style was assessed using the 30-item Children’s Report of Parent Behavior Inventory (CPRBI-30) (Schludermann and Schluderman, 1988). Mothers were classified as authoritative, authoritarian, permissive, or uninvolved/neglectful based on acceptance (α = 0.88) and control (α = 0.67) scores. As only 3.8% of mothers were classified as uninvolved, these participants were removed from analyses. Maternal and paternal logistic support (e.g., enrolling children in activities,

providing transportation to parks and playgrounds) A1210477 for physical activity and physical activity modeling were assessed using the child-completed Activity Support Scale (α > 0.7) ( Davison et al., 2003). Participants also completed four recently validated scales: (1) General Parenting Support (i.e., children’s

MLN0128 order perception of support; α, 0.8; ICC, 0.8); (2) Active Parents (children’s perceptions of their parents’ activity on both weekdays and weekend days; α, 0.7; ICC, 0.6); (3) Past Parental Activity (i.e., children’s perception of their parents’ prior physical activity level, α, 0.7; ICC, 0.6); and (4) Guiding support (i.e., parental rules for physical activity, α, 0.7; ICC, 0.7) ( Jago et al., 2009). Height and weight were measured, and a body mass index

(kg/m2) standard deviation score (BMI SDS) was calculated (Cole et al., 1995). Highest education within the household was obtained by parental Rolziracetam report. To account for the season of assessment, the hours of daylight on the first day of data collection was calculated. Analysis of variance tests with follow-up Scheffé tests were used to examine if physical activity or parenting practices differed by parenting style. Linear regression models were used to examine if parenting styles and parenting practices predicted physical activity. The model included parenting style and any parenting practice variable that was correlated (p < 0.05) with physical activity (data not reported). All models were adjusted for the highest level of education in the household, BMI SDS, and hours of daylight. Models were run separately for boys and girls. Robust standard errors were used to account for the clustering of participants within schools. All analyses were performed in Stata version 10.1 (College Station, Texas). Alpha was set at 0.05. Compared to girls, boys engaged in more minutes of MVPA per day (41.3 vs. 29.2, p < 0.001) and had a higher CPM (599.2 vs. 502.9, p < 0.001). Boys also reported higher maternal and paternal logistic support and modeling ( Table 1).

3 billion PT trips, representing a 32% increase compared to 1995. Between January and September 2008, PT usership increased, for example, by 3.8% in New York, 8.1% in Atlanta, and 32.7% in Charlotte, NC (APTA, 2008). Plans of developing a rapid rail network across the US are under discussion. The similar inflammatory and epigenetic traits observed in this study in car and PT commuters convey an important and apparently neglected prevention message that, if not integrated into a more general strategy

to achieve overall dietary and physical activity objectives, society may miss the health benefit to be harvested if commute modes increasingly are switched from car to PT. None of the authors have conflict of interests with the content of the paper. This COMIR (Commuting Mode and Inflammatory Response) project received financial support from the CUNY GSI-IX purchase Collaborative Incentive Research Grant (CIRG) program, round 16, number 1606, from the NIEHS Center ES009089 at Columbia University, and from the University of North Texas Health Science Center School of Public Health Seed Program. Results have been presented orally at the Meeting of the International Society for Environmental Epidemiology (ISEE, Barcelona, September

14, 2011). The authors thank Tashia Amstislavski and Steves Vanderpool for their help in the recruitment and data collection. “
“Cancer, cardiovascular disease, Rigosertib and diabetes affect more than half of working adults in the United States (Gulley et al., 2011 and Institute of Medicine, 2010). Two of the primary underlying causes of these and other chronic diseases in the United States are linked to behavioral and subsequent health risk factors (e.g., obesity and tobacco use that often begin in childhood) (Mokdad et al., 2004). In fact, approximately 18% of those aged 12–19 years in the United States are obese (Ogden & Carroll, 2010), and approximately 19% of high school students are current

smokers (Centers for Disease Control and Prevention [CDC], 2013). In 2010, the US Department of Health and Human Services funded the Communities Putting Prevention to Work (CPPW) project through CDC to accelerate community- and state-level policy, systems, and environmental (PSE) improvements that ultimately could Megestrol Acetate reduce the US economic burden of chronic disease by making healthy living easier (Bunnelll et al., 2012). The CPPW project addressed disparities in chronic diseases among racial and ethnic subpopulations, socioeconomic groups, and geographic settings. CDC awarded more than $400 million to 50 communities for a 2-year intervention period. In addition, evaluation was supported to examine the effectiveness of PSE improvements and to expand the evidence base. In this supplement, we expand on the work of Bunnelll and colleagues, who in 2012 reported on outcomes after the first 12 months of the CPPW program by showcasing actual CPPW community-based, data-informed strategies implemented to make healthy living easier.

Advanced Market Commitments (AMCs) for vaccines are legally-binding agreements to subsidize the purchase, at a given price, of a vaccine that is

not yet available [24]. Efforts to develop an HSV-2 vaccine date back to the 1930s [25]. They received a new momentum in the 1980s, with the emergence of biotechnology, but have so far been unsuccessful Epigenetics Compound Library [26]. However, several biotech and vaccine companies are investing in the development of an HSV-2 vaccine. Along the same line, there are no vaccines available which effectively protect against a Chlamydia trachomatis genital infection despite many efforts that have been made throughout the years since the 1950s [27]. However, several companies are now in the early phases of clinical trials or considering whether or not they should introduce chlamydia candidate vaccines into their pipeline. As for gonorrhea and trichomonas, interest does not yet seem to have reached this stage. Syphilis was not mentioned during the interviews. Decision to develop a vaccine against STIs is risky as critical scientific information is missing that renders the feasibility and the likelihood of success

of such vaccines uncertain: the mechanisms selleck screening library of protection are not known; protective antigens have to be identified, and animal models have to be developed or optimized. Moreover, the problem is compounded by the fact that the market for STIs does not seem to warrant the investment inherent in vaccine development. Successful

vaccine development has been based on an understanding of which immunological response is protective. Most successful existing vaccines rely on neutralizing antibodies [28]. Clearly, antibody responses, if necessary, are not sufficient to confer protection to STIs. The problem with HSV-2, chlamydia, gonorrhea and trichomonas is that the immunity induced by natural infection is absent or imperfect. This seriously limits the possibility of defining the types of immune responses that an effective vaccine must include. Rolziracetam What is known is that vaccines will have to do better than immunity to natural infection, but which arm of immunity is to be stimulated? There is no viral clearance of HSV-2 infection. The virus persists throughout life in a latent state in the dorsal root ganglia, with episodes of viral reactivation and shedding [29]. Immunity to natural infection by chlamydia, gonorrhea and trichomonas takes time to acquire, is incomplete and of short duration [for reviews, see 1 [30], [31] and [32], in this issue]. Repeat infections are common, and the risk of pathology is known to increase after repeated chlamydial infections [30]. The key question then becomes whether it is possible to design chlamydia vaccines that induce protective immunity without predisposing to more severe pathology.

For positive controls, HeLa/DC co-cultures were pulsed with EαGFP or EαRFP protein for 16 h. Cells were harvested, stained for CD11c and Y-Ae or CD11c and the Y-Ae isotype control (mouse IgG2b) and analysed by flow cytometry. DCs pulsed with EαGFP were Y-Ae+ (surface Eα peptide:MHC ClassII complex) ( Fig. 4B, black check details histogram), whereas both unpulsed DCs (blue histogram) and isotype controls (grey shading) show minimal staining. Flow cytometric analysis of CD11c+ cells from

plasmid-transfected HeLa/DC cultures, revealed Y-Ae+ DCs when DCs were co-cultured with pCI-EαGFP-transfectants ( Fig. 4C, black histogram) but not with pCIneo (blue histogram) or pCI-OVAeGFP (red histogram) control transfectants. Isotype controls showed little staining (grey shading). Flow cytometry results for pCI-EαRFP were similar to those for pCI-EαGFP and are not shown. Immunofluorescence staining of EαRFP protein-pulsed HeLa/DCs grown in chamber slides, clearly

demonstrated the presence of both Ag-laden cells (red) and pMHC+ (Y-Ae+) cells (green) ( Fig. 4D). Some unprocessed EαRFP can be seen in the cytosol of the Y-Ae+ cell (indicated by arrow). We also demonstrated pMHC+ cells (green) in pCI-EαRFP-transfected HeLa monolayers co-cultured with BMDCs ( Fig. 4E). In this example pCI-EαRFP-transfected HeLa cells expressing the EαRFP protein (red) can be seen adjacent to a Y-Ae+ cell (green), suggesting that the Y-Ae+ cell had acquired Ag or Eα peptide from another cell (i.e. cross-presentation). These results indicate that our Eα-based DNA vaccine constructs, PFT�� mouse in combination with the pMHC Ab Y-Ae, may be useful tools for identifying cells presenting DNA-encoded Ag in vivo. We prepared fluorescently labelled plasmid according to standard protocols,

injected labelled plasmid and attempted to identify its distribution and the phenotype of associated cells. Tissues including the TA muscle, draining popliteal and inguinal LNs, distal cervical and brachial LNs, spleen, peripheral blood and bone marrow, were collected 1 h and 24 h after however intramuscular injection of Cy5-labelled plasmid (pDNA-Cy5) or unlabelled control plasmid (pDNA). Cell suspensions and tissue sections were examined for the presence pDNA-Cy5 by flow cytometry and fluorescence microscopy (data not shown), respectively. We detected extensive Cy5+ signal in muscle 1 h after injection using fluorescence microscopy (data not shown). The signal was predominantly between muscle bundles and within myocytes, as has been shown by others previously [19]. During the preparation of the labelled pDNA we removed any unbound Cy5 by extensive washing and thus we are confident that Cy5 signal distribution corresponds with pDNA distribution. 1 h post-pDNA-Cy5 injection, we observed cell-associated pDNA-Cy5 in popliteal, inguinal and distal peripheral LNs by flow cytometry with the largest numbers found in the local muscle-draining popliteal LNs (Fig.

The solubility products (Ksp) of the formed ion-associates were determined conductimetrically 30 as described under the experimental part. The equilibrium constant of the precipitation reaction (K) is inversely proportional to the solubility product (Ksp), PD0325901 mw whereas the smaller the solubility product of the formed ion-associate, the sharper the end point ( Table 4). The solubility product of ion associate of TB-PTA is lower than that of LOP-PTA, so it is most stable. The equilibrium constants of the ion-associate formation reactions are calculated and represented as follows: 3D+ + PT−3 = D3PT. The validity of the proposed

method was assessed by its application to the determination of the investigated drugs in their pharmaceutical preparation (Triton tablets) in case of TB and Imodium capsules in case of LOP.HCl using the same procedure and conditions applied for pure solutions. From the results shown in Table 2, it is clear that the mean recovery values for Triton tablets were 99.04%, and for Imodium capsules were 99.47%. The results obtained Lumacaftor datasheet from the conductimetric determination of the drugs were subjected to statistical treatment to compare the precision of the employed technique to that methods used as references by applying F and t-tests as shown in Table 3. 29 The results shown in Table 3 are lower than the theoretical tabulated values,

i.e. the method applied does not exhibit significant difference which reflects the accuracy and precision of this method. The proposed method has the advantages of being simple, rapid, accurate and highly reproducible. It also uses simple reagents and apparatus and is applicable to a wide range of drug concentration. The proposed method is suitable for the determination of the studied drugs in dosage forms without interference from excipients such as starch and glucose or from common degradation Thymidine kinase products suggesting application in bulk drug and in dosage forms analysis.

All authors have none to declare. “
“Curculigo orchioides Gaerth, is one of the well known medicinal plant belonging to the family Hypoxidaceae (Amaryllidaceae). It is distributed widely in the southern parts of Japan, China, India and Australia, generally used as a tonic in traditional Chinese medicine to treat decline in physical strength. 1 Its rhizomes are used as an alternative for demulcent, diuretic, restorative and for the treatment of jaundice. 2 Curculigoside, an active compound isolated from C. orchioides can improve cognitive function and is developed as a new drug for the treatment of Alzheimer’s disease. 3 and 4 Despite the use of the plant in traditional, so far no scientific evaluation was carried out on this plant for the toxicity profile. Our study was therefore undertaken to screen phytochemical constituents and determine the toxicity profile of methanolic extract of root parts of Curculigo orchioides (MECO) on Wistar Albino rats.

There are plausible mechanisms related to mechanical and immunological changes that may render women more vulnerable to respiratory infections during pregnancy [4] and [5]. The European Centre for Disease Prevention and Control (ECDC) has concluded that vaccination of pregnant women could reduce the number of influenza-related hospitalizations and deaths in this group and potentially the burden of influenza in children younger than six months [6]. The WHO SAGE committee has referred to “compelling evidence of substantial risk of severe disease in

this group…” [7], and WHO has subsequently recommended pregnant women as the highest priority group for vaccination against seasonal influenza. However, a recent systematic review [8] concluded that pregnancy as a risk factor for seasonal influenza, as opposed to pandemic influenza including A(H1N1)pdm09, is not sufficiently studied. Furthermore, S3I 201 ECDC has concluded that European studies of the disease

burden of seasonal influenza in pregnant women are needed [6]. Whereas an increased risk of influenza-associated Metabolism inhibitor deaths for pregnant women has been documented during pandemics [9], [10], [11], [12] and [13], deaths in pregnant women due to inter-pandemic influenza have only been described in occasional case reports [14], [15] and [16], suggesting that this outcome is unusual. Moreover, the evidence of an increased risk of severe disease for healthy pregnant women due to seasonal, inter-pandemic influenza mainly consists of observational studies of health Oxalosuccinic acid service utilization in USA and Canada [17] and [18]. Albeit healthcare utilization often being applied as an indicator of disease severity, it should be interpreted

with caution since healthcare utilization may be context dependent. For example, despite similar symptoms and severity, there may be differences in healthcare seeking behaviour, access to healthcare or medical recommendations. Furthermore, the relative risk does not inform on burden of hospitalization, and a sufficient absolute risk is needed to motivate vaccination. Hospitalization rates of 15 and 25 per 10,000 pregnant women or third trimester women have been found in Canada and USA, respectively [17] and [18], and in a study set in the UK the rate was estimated to 13 per 10,000 pregnant women [19]. Since these rates may be context dependent and estimates in a European setting are sparse, it was deemed that a national estimate for Sweden was necessary for policy purposes. Therefore we conducted a study of hospitalizations due to seasonal, inter-pandemic influenza or respiratory infection attributable to inter-pandemic influenza among pregnant women in Sweden and assessed the number needed to vaccinate (NNV) to prevent one such hospitalization. We conducted a retrospective, register-based study of inter-pandemic seasons, using ICD-10 codes that indicate influenza hospitalizations.