Permissive parenting was associated with higher levels of physica

Permissive parenting was associated with higher levels of physical activity among 10- to 11-year-old BKM120 children. Maternal logistic support was associated with girls’ physical activity, while paternal logistic support was associated with boys’ physical activity. To promote physical activity, public health professionals could encourage parents to increase logistic support for their children’s physical activity. We have no conflicts of interest to declare. We would like to thank all of the children, parents, and schools that participated in this

study. This study was funded by a project grant from the British Heart Foundation (ref PG/06/142). This report is also a research arising from a Career Development Fellowship (to Dr. Jago) supported by the National Institute for Health Research. The views expressed in this publication are those of the authors http://www.selleckchem.com/products/chir-99021-ct99021-hcl.html and not necessarily

those of the NHS, the National Institute for Health Research, or the Department of Health. “
“Young children are often negative about smoking: they think it is unhealthy and stinks. This attitude explains why only 2% of the Dutch children aged 10–12 years smoke (STIVORO, 2008). Due to factors like smoking behavior of peers and parents, social pressure to smoke, and non-smoking policies (Bidstrup et al., 2009 and Bernat et al., 2008), this aversion to smoking diminishes rather quickly. It results in 23% smokers among 14-year olds and 44% among 18-year olds (STIVORO, 2008). Gervais et al. (2006) suggest that because a person’s first puff presents the beginning of a rapid process that leads to

symptoms of nicotine dependence and escalating cigarette use. Moreover, adolescents who are stable users of tobacco at the age of 12 show greater weekly cigarette consumption and are more likely to become nicotine-dependent (Riggs et al., 2007). The transition to high school is a period in which students are very vulnerable to factors that lead to smoking (Côté et al., 2004). This emphasizes the importance to prepare 10-to 12-year-old children before they are most apparently facing the temptation to experiment with tobacco. In a review on the efficacy of non-smoking interventions (NHS, 1999), the authors also state that an important addition to present intervention practice would be to start interventions at an earlier age, before attitudes and beliefs about smoking are being formed. Starting an education program in elementary school could therefore be an effective instrument in the prevention of smoking onset in adolescence. Flay (2009) performed a critical review of several reviews on the effects of school programs on prevention of tobacco use. There were some clear directions on what types of programs are most effective.

The interaction analysis for CID44610309, CID44259709, CID1396455

The interaction analysis for CID44610309, CID44259709, CID13964550 and quercetin is shown in Table 1. The docking simulation revealed the top docking poses were found to be docked at the binding cavity showing both bonded and non-bonded interaction. The top ten docking hits showed common interaction with Trp294

and Glu299. The snapshots of ligand–protein interaction, electrostatic interaction and the binding mode for the top docking hit CID44610309 is shown in Fig. 2. The ADME of the docking hits ranged between 0.036 and 0.28 for solubility, 3.36 × 104–7.92 × 104 for absorption and 0.59–1.12 for distribution. The LogD at various pH ranges from 1.51 to 2.81, 1.5 to 2.82, 1.43 to 2.81, 1.07 to 2.76 and 0.48 to 2.64 for stomach, duodenum, jejunum, ileum, blood and colon respectively. The percentage human oral bioavailability for the compounds ranged from 30% to 70%. Interestingly, CID44610309, selleck chemical CID44258703 and CID11834044 showed no or lesser health effects compared to the other docked compounds (Fig. 3). These three compounds could be lead molecule or a potential anti-cancer compound. The three-dimensional structure of iNOS of G. gallus was generated using Modeller 9v8. The structure assessment of the generated

model revealed the model is reliable and a quality model with stable energies. Additionally the molecular docking studies with quercetin and its analogues into the binding Forskolin mouse cavity of

iNOS showed the analogues having more favourable interaction than quercetin with favourable rerank score, docking score and hydrogen bonding energy. As quercetin is known for having anti-cancer property, the analogues docked aminophylline at the binding cavity could also possess anti-cancer property as it is 95% similar to quercetin. Interestingly, among the docked compounds the ADME–toxicity prediction revealed CID44610309, CID44258703 and CID11834044 have lesser health effects and LD50 as compared to the other docked compounds. Hence we conclude that these compounds could be a potential lead molecule and supports for experimental testing. All authors have none to declare. JPR solutions funded our article to publish. “
“Bacterial infections are leading cause of death for millions of people. This is because of the emergence of new disease agents and the development of resistant strains. Moreover, the pathogens have evolved effective approaches to counteract the biocidal action of antibiotics. Even though many antibiotics have been developed, very few antibiotics have proved effective against bacterial resistant strains. Therefore, it is extremely important to design and develop new approaches that overcome these limitations. The persistence of antibiotic resistant bacteria has renewed interest in the use of silver and silver based compounds including silver nanoparticles.

The initial phylogenetic tree of the HA1 domain nucleotide sequen

The initial phylogenetic tree of the HA1 domain nucleotide sequences of each A-subtype or B-lineage was constructed with the PhyML software package version 3.0 [4] using GTR + I + Γ4. For this analysis the general time-reversible model with the proportion of invariant sites and the gamma distribution of among-site rate variation with four categories was estimated from the empirical data, determined by ModelTest [5] as the evolutionary model.

GARLI v0.961 [6] was run on the best tree from PhyML for 2 million generations to optimise tree topology and branch lengths for each virus A-subtype or B-lineage. The virus gene sequence accession numbers and their originating laboratories used in this report are listed in Table S1. A combination of antigenic and genetic data is routinely used to identify emergent antigenic variants. Antigenic cartography [7] was used to visualise the HI data. As discussed previously, the behaviour selleck compound of A(H3N2) viruses in HA and HI assays has changed in recent years and their antigenic analyses have become more complex [8]. In particular, guinea pig RBC are now preferred for antigenic characterisation of current A(H3N2) LBH589 mw viruses in HA and HI assays. To control for the possible participation of the virus NA in the agglutination of RBC, HI assays can also be performed in the presence of oseltamivir [9]. Virus neutralisation (plaque

reduction and microneutralisation) assays were performed in addition to HI tests for a subset of A(H3N2) viruses and a small number of A(H1N1)pdm09 viruses. In addition

to antigenic studies using post-infection ferret antisera, human serum panels obtained pre- and post-vaccination with seasonal influenza vaccine formulations were used to assess current vaccine coverage against representative recently circulating viruses. Serum panels for adults, elderly and paediatric populations received from Australia, China, Japan, the UK and the USA were tested where available. Only a relatively small number of A(H1N1)pdm09 viruses (392) were subjected to HI analysis by the WHO CCs from September 2012 to February 2013. The majority of these viruses remained GBA3 antigenically closely related to the vaccine virus A/California/7/2009 based on assays with post-infection ferret antisera and only 3.3% of these viruses had reduced titres of 8-fold or greater compared to titres against the homologous virus (Table 1). A high resolution phylogenetic tree of the HA genes was constructed and included 379 A(H1N1)pdm09 isolates collected through GISRS since February 2012 as shown in Fig. S1. While the phylogenetic tree of the A(H1N1)pdm09 HA gene can be divided into eight major genetic groups, the majority of viruses analysed for the VCM belonged to group 6 with the signature amino acid (AA) substitutions D97N, S185T and S451N in HA1 (Fig. 2, Fig. S1). Fewer viruses belonged to group 7 (signature AA substitutions N97D and A197T in HA1) were still present but fewer in number than in the previous reporting period.

There were 18,002 records in the laboratory database of which 17,

There were 18,002 records in the laboratory database of which 17,783 could be matched with the hospital number to the CMS data and included in the analysis. The remaining

219 records were either not within the age range or could not be matched with their hospital number. In the 6M and 18Y groups, NPAs were requested on 2066 (24.8%) and 17,783 (39.4%) admissions (Appendix 7) and were positive in 6.5% (range 4.8–9.9%) and 13.2% (range 9.2–21.5%) during the 6 year period respectively (Appendix 8). Overall 1.6% of admissions in the 6M group and 5.2% in the 18Y group had a positive NPA for influenza (Appendix 7). In both age groups the highest positivity rate was in the 2009/10 period during which time the 2009 pandemic influenza A (H1NI) virus (A(H1N1)pdm09) influenza strain circulated but this effect was less marked in the 6M group Protein Tyrosine Kinase inhibitor (Appendix 8). In all HA hospitals the proportion of all admissions, and the proportion of admissions to general wards and intensive care units, that had a CMS diagnosis of influenza was almost double during the 2009/10 period (Appendix 9). Including all children from 0 days to below 18 years, 1993 had both a laboratory positive result and CMS diagnosis (ICD9-CM 487–487.9) of influenza (Table 1). There were an additional 359 children without a CMS diagnosis of influenza but with

a laboratory confirmed result, and 253 with a Dasatinib manufacturer CMS diagnosis of influenza but without laboratory confirmation. This indicates that a CMS diagnosis of influenza under-estimates disease burden relative to the laboratory results despite wide and routine laboratory testing with NPAs in children with fever or respiratory illnesses. Since there appeared to be no obvious age effect (Appendix 3) an overall mean value of 1.05 was used for adjustment factor 1 for all age groups. Of the Isotretinoin 11,063 children

with a primary-respiratory associated diagnosis, 1490 did not have an NPA sent. Adjustment factor 2 assumed the influenza positive rate in these 1490 children was the same as in the 9573 children that had an NPA sent (Table 1). Again this factor did not appear to vary consistently with age and overall mean value of 1.13 was applied to all age groups (Appendix 3). Adjustment factor 3 was the proportion of all admissions by age group that had a laboratory diagnosis of influenza at PWH (Table 1). This factor varied by age group and a smoothed value excluding the first two months was applied to each monthly age group for the complete HA dataset (Appendix 3). The incidence rates of hospitalisation for influenza per 100,000 person-years based on any CMS influenza diagnosis (CMS flu) for the whole of Hong Kong were lowest in the first two months of life, then peaked between 2 and 6 months, and then declined from about 3 to 4 years of age (Fig. 2 and Fig. 3). Similar patterns were observed over the full 6 years of the study.

However, little is known about the relative immunogenicity of pan

However, little is known about the relative immunogenicity of pandemic (H1N1) 2009

vaccines and how immune responses to them might be affected by prior immunization against seasonal influenza strains. In preparation for clinical studies, we initiated mouse studies designed to investigate the immunogenicity of a candidate selleck chemicals llc pandemic (H1N1) 2009 vaccine in mice in experiments designed to assess the potential requirements for use of an adjuvant, antigen dose, and the immunization regimen. In these studies, we included groups of naïve mice and mice primed against seasonal influenza strains to model the human population, which includes persons who have been primed to seasonal influenza through infection or vaccination as well as individuals with no prior exposure to influenza (usually young children). Three groups of 40 6-week-old female BALB/c mice received a single intramuscular (i.m.) injection of one of two formulations of TIV (Vaxigrip®, sanofi pasteur, Lyon, France). The first seasonal vaccine formulation (TV1) was prepared using the 2005–2006 DAPT molecular weight Northern Hemisphere formulation containing the strains A/New Caledonia/20/99 (H1N1), A/NewYork/55/2004 (H3N2) and B/Jiangsu/10/2003. The second seasonal vaccine formulation (TV2) was prepared using the 2009–2010 Northern Hemisphere formulation containing

the strains A/Brisbane/59/2007 (H1N1), A/Uruguay/716/2007 (H3N2) and B/Brisbane/60/2008. In mice, the A/New Caledonia/20/99 (H1N1) strain had been previously shown to induce low homologous hemagglutinin inhibition (HI) titers (mean < 80), while the A/Brisbane/59/2007 (H1N1) strain induced higher homologous HI titers (mean > 160) (sanofi pasteur, unpublished data). Therefore, we hypothesized that these two vaccine formulations might also differentially prime immune responses to the pandemic (H1N1) 2009 strain. Influenza-naïve control mice received injections of PBS. The use of influenza pre-immune animal models may be more representative of the effect of seasonal influenza pre-exposure in humans who are generally primed to influenza virus antigens due to prior influenza infection or vaccination. The vaccines were administered

at 1/10th of the human dose (1.5 μg of hemagglutinin (HA) per strain) to mimic the antigen dose required for the induction of residual priming in humans as reposted by Potter and Jennings [4]. Forty DNA ligase days post-TIV priming (designated as Day 0), vaccinated mice were divided into four subgroups of 10 animals each and were re-vaccinated with a monovalent inactivated pandemic H1N1 (2009) vaccine prepared using the NYMC X-179A (A/California/07/2009 H1N1) reassortant strain. Four formulations were evaluated: 3 μg HA or 0.3 μg HA, as 1/10th and 1/100th of the highest immunization doses used in clinical trials [5]; each HA dose was formulated with or without an oil-in-water emulsion adjuvant (AF03; sanofi pasteur, Lyon, France). All animals received a second injection of the identical vaccine formulation on Day 21.

Calu-3 and NHBE cell

layers were harvested from Transwell

Calu-3 and NHBE cell

layers were harvested from Transwell® inserts on the same day as 3H-digoxin permeability experiments. mRNA isolation and cDNA synthesis were performed as described previously [26]. Manual TaqMan® analysis of the ABCC7 and ABCC10-12 genes was performed in triplicate in a 25 μl reaction mixture containing 30 ng cDNA, TaqMan® Universal PCR Master Mix (containing AmpliTaq Gold DNA polymerase, dNTPs with dUTP, passive reference and optimised buffer) and Assay-on-demand™ gene expression assay mix (containing 18 μM random hexamer primers). All other genes investigated were analysed via automated Taqman® PCR low density arrays using custom designed 384-well cards as described previously [26]. Amplification curves LY2109761 were analysed using the SDS2.1 software (Applied Biosystems, Foster City, CA) and thresholds for generation of Wortmannin ic50 C  T data were calculated automatically by the software. Target genes were compared with the two house-keeping genes RPLP0 (Large Ribosomal Protein) and MVP (Major Vault Protein) ΔC  T and assigned arbitrary categories for relative gene expression levels based on the 2T-ΔC value, i.e. relative expression levels >0.5 were considered as ‘high’ (+++), 0.02–0.5 as ‘moderate’ (++), 0.001–0.02 as ‘low’ (+) and <0.001

as ‘negligible’ (−). Cells were detached from the surface of the filters/flasks by the addition of 500 μl non-enzymatic cell dissociation buffer prepared in HBSS without calcium and magnesium salts. Cells were counted and resuspended in RIPA cell lysis buffer containing 1 μl of protease inhibitor cocktail set II per 200 μl (ratio of 20 million cells per 1 ml buffer solution) and agitated at 700 rpm at 4 °C for 30 min. Cell debris was pelleted at room temperature by centrifugation at 12,000g for 20 min and the resulting supernatant decanted. Protein concentration was quantified using the RC DC™ protein assay (BioRad, Hemel Hempstead,

Hertfordshire). Protein samples were resolved using 7% Tris–acrylamide gels. Briefly, 10 μl of cell lysate solution containing 20–30 μg Rebamipide of protein was diluted 1:1 with reducing sample buffer. Samples were run under denatured and reduced conditions alongside 5 μl precision plus protein standards (BioRad, Hemel Hempstead, UK) and resolved at 0.04 amps in running buffer. Transfer to a nitrocellulose membrane was conducted for 60 min at 100 V and at a temperature of 4 °C. Proteins transferred onto Western blots were visualised by staining with copper phthalocyanine 3,4′,4″,4″′-tetrasulphonic acid tetrasodium salt (CPTA). Samples were probed for the presence of MDR1 protein using 5 μg/ml of the mouse anti P-glycoprotein C219 primary antibody (Calbiochem, Nottingham, UK) for 16 h at 4 °C. All steps were performed using a chemiluminescence detection kit according to the manufacturer’s instructions (Invitrogen, Paisley, UK).

The standard primer sets VP7F/R and Beg9/End9 were used to amplif

The standard primer sets VP7F/R and Beg9/End9 were used to amplify VP7, VP4F/R and Con2/Con3

to amplify the VP8* subunit of the VP4 gene and 10.1/10.2 to amplify NSP4 [20], [21] and [22]. PCR amplicons were purified using Selleck Galunisertib the QIAquick Gel extraction Kit (Qiagen, Inc., Hilden, Germany) according to the manufacturer’s protocol. Purified cDNA was sequenced using BigDye Sequencing Kit version 3.1 (Applied Biosystems; Foster City, CA, USA) in both directions using the oligonucleotide primer sets used in the gene amplification PCR protocol. The thermal cycling reaction consisted of 30 cycles of 96 °C for 15 s, 50 °C for 10 s and 60 °C for 4 min and the products purified by ethanol precipitation. The nucleotide sequence was determined by Applied Genetic Diagnostics (University of Melbourne, Victoria, Australia), using an ABI 3130xl Genetic Analyser (Applied Biosystems, Foster City, CA, USA). Sequence data were analysed utilising the Sequencher® Software program version 4.1 (Gene Codes Corp Inc., Ann Arbor, MI, USA). Sequence identity was determined using the BLAST (Basic Local Alignment Search Tool)

server on the GenBank database at the National Centre for Biotechnology Information, USA (www.ncbi.nlm.nih.gov). Sequences from this study and those obtained from the GenBank MG-132 order database were aligned using ClustalW [23]. Genetic distances were calculated using the Kimura-2 correction parameters at the nucleotide level and phylogenetic trees were constructed using the Neighbor-joining method with 500 bootstrap replicates utilising the program MEGA version 4 [24]. The nucleic acid sequences for genes described in this study have been deposited in GenBank (Accession numbers JN377704-JN377721). For simplicity, samples will be referred to by abbreviate common names, AS07-obV2, AS07-obV12, AS07-obV18, AS07-obV37, AS07-obV42, AS07-obV50,

AS07-obV57, AS07-obV75, AS07-obV93, and AS07-obV121. A total of 107 stool samples were collected during a large gastroenteritis outbreak in Alice Springs (Northern Territory) were sent to the Australian Rotavirus Reference Centre for genotype analysis. Seventy-eight samples were found to be rotavirus positive. through Sixty-five samples were analysed by PAGE and silver stained to allow the visualisation and comparison of the electrophoretic pattern. An RNA electropherotype was visible in 57 samples; all samples displayed an identical long electropherotype (data not shown). Fourteen G9P[8] samples from the outbreak were selected for sequence analysis, including two samples from vaccinated infants. The coding region of the VP7 gene was determined for each of the 14 samples, and revealed a highly conserved gene, which displayed 99.9–100% nucleotide homology and 99.6–100% amino acid identity to each other. No conserved amino acid changes were observed between samples obtained from vaccinated and non-vaccinated patients.

Reported PPV in studies performed on mixed high- and low-risk pop

Reported PPV in studies performed on mixed high- and low-risk populations, as well as the current study, far exceed current screening methodologies. Consistent with this, recent guidelines published by the American College of Medical Genetics and Genomics (ACMG) do not distinguish between high and low risk. Therefore, the transition of NIPT into a universal, first-line, aneuploidy screen should depend on the availability and affordability of NIPT, and not concerns about performance. In this cohort of women who were thought to have singleton

pregnancies at the time of NIPT, 127 cases were identified as having >2 fetal haplotypes suggesting either triploidy or a previously undetected multifetal pregnancy or vanishing twin. The SNP-based NIPT methodology provided the opportunity Cell Cycle inhibitor to identify these cases, pursue further diagnostic avenues, and avoid FPs that can arise using alternative methodologies.22 The main limitation of this study is the incomplete follow-up data, particularly on low-risk patients, precluding precise calculation of sensitivity and specificity. While follow-up was not conducted on low-risk patients, given the clinical significance of a FN report, and based on our laboratory

experience, it is likely that FNs would be voluntarily reported; there were 2 voluntarily reported FNs. However, the lack of comprehensive follow-up on all low-risk patients precluded determination of the negative predictive value. Oxymatrine Nevertheless, it is important to note that strong performance characteristics were in keeping with GSK2118436 prior validation studies,2, 3 and 24 even with the inclusion

of mosaic samples. Follow-up of normal results remains an issue for all laboratories that wish to track results for quality assurance, and we support the ACMG recommendation for a national registry.16 In conclusion, this is a large-scale report of clinical utilization of NIPT. Analysis of >31,000 samples from both low- and high-risk women supported that test performance of this NIPT method in a clinical setting mirrors the robust performance reported in validation studies. Clinical performance of SNP-based NIPT in a mixed high- and low-risk population is consistent with performance in validation studies. Similar PPVs were found in women aged <35 years and aged ≥35 years. The strength of the study is the robust information it provides on clinical application of NIPT. The primary limitation is the incomplete follow-up data, particularly on low-risk patients, precluding precise calculation of sensitivity and specificity. This study supports the use of NIPT as a first-line screening test for aneuploidy in all patients. Furthermore, it highlights the importance of, as well as provides data that can improve, counseling of patients.

13 One of the difficulties in evaluating the evidence is that so

13 One of the difficulties in evaluating the evidence is that so few studies in this area have been randomised controlled trials. The lack of controlled trials is a problem because apart from there being an increased risk of bias in the results, other factors that could influence outcomes, such as the amount of physiotherapy, may not be controlled or accounted for. A key issue in evaluating the effectiveness of out-of-hours physiotherapy services is determining whether

the NVP-BEZ235 services provided are additional services, or whether they are redistributed from existing Monday-to-Friday services.3 There is strong evidence that providing additional physiotherapy across a range of health conditions and across acute hospital and rehabilitation settings can improve patient outcomes and reduce length of stay.14 Out-of-hours services are one way of increasing the amount of physiotherapy provided to patients. In the context of providing additional physiotherapy services, it has also been reported that rehabilitation inpatients had a different attitude to treatment when services were provided at the weekend; they considered that they were there to work, whereas the attitude of patients receiving a 5-day service was ATM Kinase Inhibitor mouse that rest was more important at the weekend.15 Perhaps the key benefit of an out-of-hours physiotherapy service is that it provides an opportunity to increase the intensity of therapy provided.7 This benefit

may not manifest if the overall amount of physiotherapy is not increased by the redistribution of a 5-day service over 7 days. As a member of a multidisciplinary team, it may be a problem if the physiotherapist is providing out-of-hours service, but the other members of the team are not. For example, in a retrospective study where only the physiotherapy service was increased at the weekend, the physiotherapy length of stay decreased but the hospital length of stay did not.14 The main

issue identified for this discrepancy was that other parts of the health service were not ready for patient discharge. Consistent with this, other allied health professions such as social work and occupational therapy, which are essential to patient management and discharge planning, typically have much lower weekend coverage than physiotherapy.6 unless This issue of recognising that one area of the health service cannot function effectively at the weekend without having access to other areas of the health service has been more broadly recognised in a discussion about providing a 7-day service in the National Health Service in the United Kingdom.16 Another issue is whether the efficacy of a particular physiotherapy intervention has been established with 5-day or 7-day input. For example, all four trials of inspiratory muscle training to facilitate weaning from artificial ventilation in the intensive care unit have provided the physiotherapist-administered training on a 7-day basis.

Adding Rota created new transport (e g , between the Natitingou D

Adding Rota created new transport (e.g., between the Natitingou Department and the Parakou Department and the Kandi Region Store

and the Parakou Department) and storage bottlenecks (several Department and Commune Stores now had insufficient capacity) and lowered vaccine availability, increased transport operating costs (without affecting other operating costs) and decreased doses delivered, increasing the logistics cost per dose administered from $0.23 to $0.26. As Table 2 shows, a total capital expenditure of $285,088 (two cold rooms ($58,502) and one building selleckchem ($26,686) at the National Depot, three cold rooms ($87,753) and two buildings to house the cold rooms ($37,146) at the Department level, 17 refrigerators ($51,000) at the Commune level, and eight refrigerators ($24,000) at the Health Posts level) would be needed to alleviate current bottlenecks to drop the logistics cost per dose administered to $0.20. At the lowest level, replacing the point-to-point motorcycle

routes with 4 × 4 truck transport loops (Table 1) results in fewer total trips (a truck, which can carry more vaccines and serve more Health Outposts than a motorcycle, would only have to travel once monthly versus two to three times a month) but a higher recurring MAPK inhibitor transportation cost ($0.36 versus $0.10 per kilometer) since longer distance truck transport loops incur Isotretinoin more per diems. Adding more Health Posts per truck loop further decreases the total distance traveled but the increased distance per loop may incur more per diems. Simply adding shipping loops to the current structure did not yield cost savings (Table 3). With the existing vaccine regimen, consolidating the Commune level into 34 Health Zones (by redistributing existing Commune level equipment rather than purchasing new equipment) slightly increased

overall vaccine availability, increased transport costs (from increasing route distances), and lowered labor costs (from fewer locations requiring fewer total personnel). Rota introduction dropped vaccine availability from 94% to 64%, and increased logistics cost per dose from $0.23 to $0.29 (a greater increase than for the current baseline structure, $0.23 to $0.26). Absorbing the former Communes’ demand further constrained the transport routes to the Health Zones. Alleviating the bottlenecks for the Health Zone structure required less new equipment (two cold rooms and one building at the National Depot, three cold rooms and two buildings at the Department level, and eight refrigerators at the Health Posts) and therefore lower capital expenditures than doing so for the current Benin structure, since having fewer locations allowed reassignment of many cold storage devices.