Whether preBötC SST neurons represent a functionally specialised population is unknown. We tested the effects on respiratory and vocal behaviors of eliminating SST neuron glutamate release by Cre-Lox-mediated genetic ablation of the vesicular glutamate transporter 2 (VGlut2). We found the targeted loss of VGlut2 in SST neurons had no effect on viability in NVP-AUY922 solubility dmso vivo, or on respiratory period or responses to neurokinin 1 or μ-opioid receptor agonists in vitro. We then compared medullary SST peptide expression in mice with that of two species that share extreme respiratory environments

but produce either high or low frequency vocalisations. In the Mexican free-tailed bat, SST peptide-expressing neurons extended beyond the preBötC to the caudal pole of the VII motor

nucleus. In the naked mole-rat, however, SST-positive neurons were absent from the ventrolateral Everolimus molecular weight medulla. We then analysed isolation vocalisations from SST-Cre;VGlut2F/F mice and found a significant prolongation of the pauses between syllables during vocalisation but no change in vocalisation number. These data suggest that glutamate release from preBötC SST neurons is not essential for breathing but play a species- and behavior-dependent role in modulating respiratory networks. They further suggest that the neural network generating respiration is capable of extensive plasticity given sufficient time. “
“Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by progressive loss of dopaminergic (DAergic) neuronal cell bodies in the substantia nigra pars compacta and gliosis. The cause and mechanisms underlying the demise of nigrostriatal DAergic neurons are ill-defined, but interactions between genes and environmental factors are recognized to play a critical role in modulating the vulnerability to PD. Current evidence points to reactive glia as a pivotal factor in PD pathophysiology, playing Amylase both protective and destructive

roles. Here, the contribution of reactive astrocytes and their ability to modulate DAergic neurodegeneration, neuroprotection and neurorepair in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) rodent model of PD will be discussed in the light of novel emerging evidence implicating wingless-type mouse mammary tumor virus integration site (Wnt)/β-catenin signaling as a strong candidate in MPTP-induced nigrostriatal DAergic plasticity. In this work, we highlight an intrinsic Wnt1/frizzled-1/β-catenin tone that critically contributes to the survival and protection of adult midbrain DAergic neurons, with potential implications for drug design or drug action in PD.

The bacterial cell surface

is different between the two serovars, as represented by various O:H:K antigens. Lipopolysaccharide differences (O antigen) allowed the classification of S. Typhimurium in serogroup B, while S. Typhi belongs to serogroup D. Only S. Typhimurium is capable of phase variation of its H antigen, by differential expression of two flagella subunits. The most important feature is undoubtedly the presence of a polysaccharidic capsule (K antigen) specific to S. Typhi, the Vi antigen. However, it is also interesting ICG-001 to note that some S. Typhi strains and S. Paratyphi A lack the Vi antigen, but both cause a disease very similar to S. Typhi in the human host (McClelland et al., 2004; Baker et al., 2005). Virulence factors can be secreted using the general secretion machinery of the bacteria or by specific systems, such as the T3SS used to inject proteins directly into the host. No major differences were observed in both T3SS (Fig. S1a,b), Gefitinib but some of the effectors were missing in S. Typhi (Table S1). However, the T6SS included on

SPI-6 is probably inactivated in S. Typhi by the presence of pseudogenes. Some toxins were specific to S. Typhimurium, such as SpvB present on the virulence plasmid. On the other hand, the CdtB and ClyA toxins are only produced by S. Typhi. Interestingly, most of the genes involved in intestinal colonization identified in S. Typhimurium are inactivated in S. Typhi. These genes encode autotransporters MisL and ShdA, adhesin SiiE, secreted protein RatB, putative outer membrane protein SinH and Lpf fimbriae (Fig. 1), suggesting that they are not needed by S. Typhi in the human host. This particular divergence is further acknowledged when looking at some work involving vaccine development (DiPetrillo et al., 1999; Angelakopoulos & Hohmann, 2000; Hindle et al., 2002). Salmonella enterica serovar Typhimurium and S. Typhi live-attenuated vaccine strains, both HSP90 modified with the same genetic deletions, did not show the same level of intestinal colonization when administered orally to human

volunteers. Prolonged bacterial shedding by the host was observed over time with S. Typhimurium, but not with S. Typhi. Thus, precautions must be taken when extrapolating the S. Typhimurium data to S. Typhi. Many clinical trials investigating novel S. Typhi vaccine strains harbouring mutations that render S. Typhimurium avirulent and immunogenic in mice led to disappointing results at the attenuation level when administered to humans (Hone et al., 1988; Tacket et al., 1992a, b). The completion of additional genome sequencing projects of other Salmonella serovars or strains will contribute considerably to our understanding of niche adaptation and bacterial evolution in general, as well as conceiving the molecular basis of epidemics and how new virulent strains emerge. However, the availability of whole-genome sequences of several strains of different S.

Thus, in the case that the population structure can be described by the clonal replacement model, most mutations are lost and only one mutation can become established leading to one selective sweep at a time; therefore, the population is assumed to be homogeneous except

during the periods when the beneficial mutant is sweeping through the population. The second theory is called clonal interference (Fig. 1b) or sometimes called one-by-one clonal interference because buy Lumacaftor it is assumed that only one mutation can become fixed at a time. This occurs when mutations are established faster than the rate of fixations, multiple beneficial mutants can coexist and compete against each other until the one with the greatest fitness Gefitinib mouse advantage outcompetes all the other

genotypes and become the next founding genotype for subsequent evolution. The population is thus heterogeneous except immediately after the complete sweep by the fittest mutant. This theory focuses on the competition between mutations with different fitness effects (Gerrish & Lenski, 1998; Orr, 2000; Gerrish, 2001; Kim & Stephan, 2003; Campos & de Oliveira, 2004; Wilke, 2004) and assumes that mutations cannot be stacked in the same genetic background before the fixation of the most-fit mutation. However, the size of a typical laboratory microbial population is large enough to support multiple beneficial mutations occurring in same lineage before the first mutation in that lineage can fix (Desai & Fisher, 2007), which is the basis of the third theory: the ‘multiple-mutation’ model (Desai et al., 2007) (Fig. 1c). Multiple theoretical and experimental studies in other organisms have indirectly suggested the importance of this multiple-mutation effect (Yedid & Bell, 2001;

Shaver et al., 2002; Bachtrog & Gordo, 2004). A study using Saccharomyces cerevisiae evolving under carbon source limitation showed experimental support for this theory (Desai et al., 2007). Therefore, depending on the size of the population, the rate of mutation, time required for the establishment of a beneficial mutation, the fitness distribution of the mutations, and other important factors, evolution dynamics HSP90 in C. albicans during long-term exposure to antifungal agents may be described by one, or combinations, of the theories mentioned above. Because without exact genotype information, it is difficult to differentiate between the one-by-one clonal interference model and the multiple-mutation model, we will use the general term clonal interference to describe a heterogeneous evolving population structure. In the seminal paper on C. albicans adaptive evolution during antifungal drug exposure, Cowen et al. (2000) evolved 12 parallel populations, six in the absence and six in the presence of fluconazole for 330 generations, and isolated clones throughout the course of the evolution.

They were instructed to ignore the auditory stimulation and watch a Regorafenib datasheet silenced, subtitled movie of their choice on a computer screen in front of them (distance = 120 cm). Figure 1 schematically pictures the experimental design. Stimulus-onset asynchrony (SOA) was set to 150  ms. The onset of first deviant tones was always unpredictable, and violated in the pitch dimension the first-order formal regularity established by standard

tone repetition. We assume that also the repeated deviant tone violated the first-order regularity established by standard tones. In both cases, a first-order prediction error response is elicited. Two ‘repetition probability’ conditions were created: in a ‘high-repetition probability’ condition, deviant tones were always repeated; in a ‘low-repetition probability’ condition, deviant tones were either repeated or followed by a standard tone with equal probability. Two ‘temporal regularity’ conditions were created, producing ‘isochronous’ and ‘anisochronous-onset’ sequences. Large jitter values may induce significant differences in single-trial peak latencies, leading to an artifactual reduction of event-related deflection amplitudes (low-pass effect of averaging procedure; see Spencer, 2005). We thus kept anisochrony to a perceptible minimum, limiting the SOA jitter to ± 20% (in randomized steps of 5 ms, range 120–180 ms, uniform distribution). The same number of deviant pairs was used

in both deviant repetition probability conditions. In the high-repetition probability mTOR inhibitor condition, there were 1200 standard and 240 deviant stimuli, accounting for 120 deviant pairs. Standard tones had a probability of 83.33%, and deviant tones 16.67% (each deviant considered as a single event). They were administered in one block of about 3.6 min. In the Adenosine low-repetition probability condition, global oddball values were adapted to 87% standard and 13% deviant tones: 2400 standard, 360 deviant stimuli, accounting for 120 deviant pairs and 120 single deviant tones (one block, about 6.9 min). This way, we could control for refractoriness-dependent

differences on the elicitation of first deviant N1 amplitudes, as the length of standard sequences (mean n = 10) before first deviant onset was the same across higher-order formal regularity conditions: high-repetition probability, 1200 standards/120 first deviants; low-repetition probability, 2400 standards/240 first deviants, pooled from both paired and single events. Block order presentation was randomized within subjects. An additional condition with repetition probability set to 75% was also included. Its effects are reported in the Supporting Information, section A, as they were uninformative to the aims of distinguishing between high and low deviant repetition probabilities. Electroencephalogram (EEG) was continuously recorded using an ActiveTwo amplifier system (BioSemi, Amsterdam, the Netherlands; http://www.biosemi.

, 2003; Grüner et al., 2004; Cowman & Crabb, 2006; Iyer et al., 2007a, b). Little is known about how the large RH transmembrane proteins mediate their function during erythrocyte invasion, but a crucial step appears to be the proteolytic cleavage during the invasion process (Ogun & Holder, 1994; Triglia et al., 2009). Members of RH have been identified in all Plasmodium species analyzed so far, indicating the conserved function and importance of this protein family to the

malaria parasite (Iyer et al., 2007a; Rodriguez et al., 2008). In the rodent malaria parasite Plasmodium yoelii, Epigenetics Compound Library datasheet which has been widely used as a model to study host–parasite interactions (Landau & Gautret, 1998), the RH protein, termed Py235 (235 kDa in mass), has been shown to be a potential virulence factor that allows the parasite to invade a wider range of host erythrocytes (Freeman et al., 1980; Holder & Freeman, 1981). Py235 is also involved in the clonal phenotypic variation of merozoites (Preiser et al., 1999), enabling the parasite to evade immune responses and adapt to changes in Alectinib in vivo the host environment during the invasion step (Snounou et al., 2000). Previously, a 94 kDa domain of Py235 of P. yoelii, which is highly conserved among the RBLs, has been found to selectively bind ATP and ADP, and is termed the nucleotide-binding domain (NBD94, Ramalingam et al., 2008). The amino acid sequence

483FNEIKEKLKHYNFDDFVKEE502 in NBD94 has been identified as a nucleotide-binding region as shown by photoaffinity labeling of the nucleotide analogue 8-N3-3′-biotinyl-ATP (Ramalingam

et al., 2008). The preference of MgATP over MgADP recognition is associated with specific structural alterations in the C-terminal domain of NBD94 as depicted by spectroscopic comparison of NBD94 and its C-terminal truncated form, NBD941–550, in which no nucleotide-dependent alteration could be observed (Ramalingam et al., 2008). This nucleotide effect in the recombinant protein is potentially significant, as demonstrated by a strong binding of Py235 to RBCs in the presence of MgATP, which becomes considerably reduced either in the presence of MgADP or in the absence of nucleotides this website (Ramalingam et al., 2008). Based on these traits and the absence of significant ATPase activity of NBD94, this domain was suggested to serve as an ATP/ADP sensor during the invasion process (Ramalingam et al., 2008). More recently, the low-resolution solution and crystallographic structure of the smallest structural unit, able to bind nucleotides, and its coupling module, the hinge region, have been determined, respectively (Grüber et al., 2010). The crystal structure of the hinge region, including residues 566–663, called NBD94566–663, consists of two helices 97.8 and 48.6 Å in length, linked by a loop. The region NBD94444–547 (residues 444–547 of NBD94) has been identified to form the nucleotide-binding segment, specific for ATP and ADP.

Patients’ warfarin knowledge was assessed at 8 and 90 days post-discharge using the Oral Anticoagulation Knowledge test. One hundred and thirty-nine patients were recruited into the usual care group between November 2008 and August 2009, and 129 into the intervention group between May and December

2009. Pharmacist-delivered warfarin education was associated with a significant difference between the intervention patients’ baseline and day 8 mean warfarin knowledge scores of 64.5% (95% confidence interval (CI) 61.0–68.5%) and 78.0% (95% CI 74.5–81.5%; P < 0.001), respectively. The intervention patients also scored significantly higher than the usual care patients at day 8 (65.0%, 95% CI 61.5–68.0%; this website P < 0.001), but not at day 90. Use of an existing healthcare framework overcame several systemic barriers by facilitating warfarin education in patients’ homes. While the intervention was associated with better short-term warfarin knowledge, follow-up may be required to optimise its benefits. Widespread implementation of home-based warfarin education by pharmacists has the potential to contribute significantly to improved outcomes from warfarin therapy. "
“The National

Institute for Torin 1 in vivo Health and Clinical Excellence/National Patient Safety Agency (NICE/NPSA) guidelines for medicines reconciliation (MR) on admission Celecoxib to hospital in adult inpatients were introduced

in 2007, but they excluded children less than 16 years of age. We conducted a survey of 98 paediatric pharmacists (each from a different hospital) to find out what the current practice of MR in children is in the UK. Responses showed that 67% (43/64) of pharmacists surveyed carried out MR in all children at admission and only a third 34% (22/64) had policies for MR in children. Of the respondents who did not carry out MR in all children, 80% (4/5) responded that they did so in selected children. Pharmacists considered themselves the most appropriate profession for carrying out MR. When asked whether the NICE guidance should be expanded to include children, 98% (54/55) of the respondents answered ‘yes’. In conclusion, the findings suggest that MR is being conducted inconsistently in children and most paediatric pharmacists would like national guidance to be expanded to include children. “
“Aim  The primary objective was to analyse reported dispensing errors, and contributing factors, in Scottish National Health Service hospitals by coding and quantifying error reports from the DATIX patient-safety software. The secondary objective was to gather managerial responses to dispensing error in order to gain a perspective on interventions already in place. Methods  Incident reports collected from 23 Scottish hospitals over a 5-year period were analysed retrospectively.

Currently, instituting a second pharmacy check of PTTAs is not warranted. 1. Dodds LJ.

Pharmacist contributions to ensuring safe and accurate transfer of written medicines-related discharge information: lessons from a collaborative audit Mitomycin C datasheet and service evaluation involving 45 hospitals in England. Eur J Hosp Pharm Published Online First: 10 February 2014. doi:10.1136/ejhpharm-2013-000418 K. Medlinskiene Hull and East Yorkshire NHS Hospitals, Hull, UK HDS is the main communication tool between hospital and general practitioners. Evaluate turnaround time for HDS and to what extent pharmacist input was required. The average turnaround time for HDS in the pharmacy was 2 h 22 min and 75% of HDS required pharmacist input. The hospital discharge summary

check details (HDS) is the main method of communicating patient’s diagnostic findings, hospital management, and arrangements for post-discharge follow up to general practitioners. HDS are additionally checked by hospital pharmacists if discharge medication supply is required. It is not unusual to receive complaints from patients about long waiting times for discharge medication. The study aimed to evaluate average time of a HDS journey and extent to which pharmacist input was required. The data collection was performed during one week in November 2013 at one of three acute NHS Trust sites. All HDS received in the pharmacy had forms attached for time recordings (time a HDS was created, reached the pharmacy,

turnaround time in the pharmacy). Data from HDS with completed time recordings was retrospectively analysed with Microsoft Excel to evaluate if pharmacist input was required. Any interventions, contributions and adjustments to HDS e.g. dose changes, additional instructions, completion of stopped medication box, completion of allergy status, were classed as pharmacist input. Ethical approval was not required. A total of 196 HDS had completed forms which represented 62% (314) of all HDS received that week MG-132 price by the pharmacy. The average time for one HDS to reach the pharmacy once it had been created was 1 h 4 min. Only 5% (10) HDS were in the pharmacy 24 h prior discharge as per trust policy.1 The average turnaround time for a HDS was 2 h 22 min, which was considerably lower on the weekend (1 h 18 min). Each HDS was collected or delivered to the ward on average within 33 min. The overall average time of HDS journey was 3 h 59 min. The majority of HDS, 75% (147), required pharmacist input. Pharmacist input was achieved by using information on inpatient drug cards, contacting ward (nurse or doctor), or both (Table 1). Table 1 Sources used for pharmacists input Drug card 70% (103) Contacting ward (doctor or nurse) 2% (3) Both 28% (44) HDS are mostly written by junior doctors and errors are often associated with this junior status.

4). Patients who were virally suppressed for <50% of the time they were on cART had almost a 3-times higher rate of virological failure compared with patients who were virally suppressed for >90% of the time they were on cART (IRR 2.91; 95% CI 2.23–3.81; P<.0001). In addition to the variables describing the patients' history of viral suppression prior to baseline, demographic variables found in univariate analysis to be associated with rate of virological failure after

baseline were gender, age, HIV exposure group, region of Europe, hepatitis C status, ARV exposure status (naïve or experienced) at cART initiation, whether AIDS had been diagnosed previously, CD4 nadir, time on cART prior to baseline, number of ARVs to which the patient was exposed prior to baseline, date of baseline, treatment regimen at baseline, Inhibitor Library order the reason for the switch in treatment at baseline and the number of new drugs selleck chemicals llc started. After adjustment (Table 2), there was no significant difference in the rate of virological failure between patients whose last viral rebound was more than 3 years prior to baseline and patients who had never rebounded (IRR 1.06; 95% CI 0.75–1.50; P=0.73), whereas patients who had virally rebounded in the year prior to baseline had a 2.4-times higher rate

of virological failure after baseline than patients who had never rebounded (IRR 2.40; 95% CI 1.77–3.26; P<0.0001). The lower the percentage of time a patient had spent virally suppressed prior to baseline, the higher the rate of virological failure; patients who had spent <50% of the time they were on cART prior to baseline with a suppressed viral load had an 86% (IRR 1.86, 95% CI 1.36–2.55; P<.0001) higher rate of virological failure after baseline compared with patients who were suppressed >90% of the time they were on cART. Older patients had a lower rate of virological failure (IRR 0.84 per 10 years older; 95%

CI 0.75–0.94; P=0.0003). Patients with a higher CD4 nadir had an increased rate of virological failure (IRR 1.13 per two-fold increase; 95% CI 1.03–1.22; P=0.0009). In addition, the more ARVs a patient had been exposed to prior to baseline, the higher the rate of virological failure (IRR 1.06 per drug; 95% CI 1.01–1.12; P=0.03). Patients on a boosted PI-containing cART regimen had a 24% lower rate of virological failure (IRR 0.76; 95% CI 0.57–1.01; Suplatast tosilate P=0.06) and patients on an NNRTI regimen had a 31% lower rate of virological failure (IRR 0.69; 95% CI 0.53–0.90; P=0.007) compared with patients on a nonboosted PI regimen. The analyses were repeated with virological failure defined as two consecutive viral load measurements > 500 copies/mL. Two hundred and seventy-eight patients (15%) experienced confirmed virological failure after baseline, with an IR of 4.2 per 100 PYFU (95% CI 3.7–4.7). After adjustment, patients who were virally suppressed <50% of the time they were on cART had a 2.4-times higher rate of virological failure (95% CI 1.58–3.

4). Patients who were virally suppressed for <50% of the time they were on cART had almost a 3-times higher rate of virological failure compared with patients who were virally suppressed for >90% of the time they were on cART (IRR 2.91; 95% CI 2.23–3.81; P<.0001). In addition to the variables describing the patients' history of viral suppression prior to baseline, demographic variables found in univariate analysis to be associated with rate of virological failure after

baseline were gender, age, HIV exposure group, region of Europe, hepatitis C status, ARV exposure status (naïve or experienced) at cART initiation, whether AIDS had been diagnosed previously, CD4 nadir, time on cART prior to baseline, number of ARVs to which the patient was exposed prior to baseline, date of baseline, treatment regimen at baseline, Selumetinib ic50 the reason for the switch in treatment at baseline and the number of new drugs Ku-0059436 manufacturer started. After adjustment (Table 2), there was no significant difference in the rate of virological failure between patients whose last viral rebound was more than 3 years prior to baseline and patients who had never rebounded (IRR 1.06; 95% CI 0.75–1.50; P=0.73), whereas patients who had virally rebounded in the year prior to baseline had a 2.4-times higher rate

of virological failure after baseline than patients who had never rebounded (IRR 2.40; 95% CI 1.77–3.26; P<0.0001). The lower the percentage of time a patient had spent virally suppressed prior to baseline, the higher the rate of virological failure; patients who had spent <50% of the time they were on cART prior to baseline with a suppressed viral load had an 86% (IRR 1.86, 95% CI 1.36–2.55; P<.0001) higher rate of virological failure after baseline compared with patients who were suppressed >90% of the time they were on cART. Older patients had a lower rate of virological failure (IRR 0.84 per 10 years older; 95%

CI 0.75–0.94; P=0.0003). Patients with a higher CD4 nadir had an increased rate of virological failure (IRR 1.13 per two-fold increase; 95% CI 1.03–1.22; P=0.0009). In addition, the more ARVs a patient had been exposed to prior to baseline, the higher the rate of virological failure (IRR 1.06 per drug; 95% CI 1.01–1.12; P=0.03). Patients on a boosted PI-containing cART regimen had a 24% lower rate of virological failure (IRR 0.76; 95% CI 0.57–1.01; Flavopiridol (Alvocidib) P=0.06) and patients on an NNRTI regimen had a 31% lower rate of virological failure (IRR 0.69; 95% CI 0.53–0.90; P=0.007) compared with patients on a nonboosted PI regimen. The analyses were repeated with virological failure defined as two consecutive viral load measurements > 500 copies/mL. Two hundred and seventy-eight patients (15%) experienced confirmed virological failure after baseline, with an IR of 4.2 per 100 PYFU (95% CI 3.7–4.7). After adjustment, patients who were virally suppressed <50% of the time they were on cART had a 2.4-times higher rate of virological failure (95% CI 1.58–3.

0. The study was approved by the Bronx-Lebanon Hospital Center Institutional Review Board. A total of 129 parents (93% mothers) with a median BAY 57-1293 age (range) of 29.0 (18–60) years were eligible and agreed to participate. Most originated from West Africa (110, 85%), particularly Ghana (24, 19%), followed

by Latin America/Caribbean (12, 9%), and Asia (7, 5%). The mean time (SD) of stay in the United States since immigration was 6.2 (4.7) years. A total of 20 (16%) had a college degree, 18 (14%) had attended college without receiving a degree, 31 (24%) were high school graduates without additional schooling, 47 (36%) attended school without receiving a high school degree, the remaining 13 (10%) received no schooling. About half (61, 47%) had access to the Internet at home. The median number of children per family (range) was 2 (1–9), and in approximately a quarter of the families (31, 24%) at least one child was living in the parent’s country of origin. Forty-seven of the parents interviewed (36%) had plans to travel within the next 12 months, whereas 19 (15%) and 6 (5%) parents planned to travel within the next 3 or 5 years, respectively. An additional 45 (35%) parents had plans to travel but could not specify how soon they intended to go. Only 12 (9%) had no plans to travel at the time of the interview. Among those with plans to travel within 12 months, the majority (36, 77%) intended to stay >1 month

and 5 (11%) >6 months. Country of birth in Ghana was the only factor buy PD-0332991 found to be significantly associated with an intention to travel within the next year (Table 1). Thirty-three (26%) had traveled back to their country of origin at least once since immigration, Thymidine kinase of whom 62% reported having a pre-travel encounter, but only 43% had taken malaria chemoprophylaxis. With regards to malaria-relevant KAP, 96% of parents recognized that malaria is a mosquito-borne disease, but 20% also considered exposure to unclean water as an important risk factor. The majority knew that malaria causes fever (92%), can be fatal (81%), and that taking medication was one way to prevent

it (71%). However, only 57% identified the protective benefits of combining chemoprophylaxis and mosquito repellents. Higher education (at least high school graduate) was significantly related to knowledge about malaria’s potential lethality (p < 0.03) and the protective effect of insecticides (p < 0.05), but not to knowledge about repellents (p < 0.1) or chemoprophylaxis (p = 0.7). Many literature reports have commented on the low proportion of VFRs who receive pre-travel advice and on how important it is that new and innovative methods be developed to enhance the opportunities for VFRs to access a pre-travel visit.1–5,8 This study, to the best of our knowledge, is the first to evaluate screening for high-risk travel among immigrant families from malaria-endemic countries during a routine pediatric health maintenance visit.