, 2008; Kabashi et al., 2008b; Sreedharan et al., 2008; Yokoseki et al., 2008). TDP-43 is a widely-expressed 414-amino-acid protein encoded by the TARDBP gene on chromosome 1 (Pesiridis et al., 2009; Geser et al., 2010). It has two RNA-binding domains and a glycine-rich domain in the C-terminal part, with which it binds

to various heterogenous nuclear nucleoproteins (hnRNPs). It is more abundantly present in the nucleus than in the cytoplasm. The exact role of TDP-43 is incompletely understood, but it is thought to play a role in a variety of processes such as processing, stabilisation and transport of RNA (Buratti & Baralle, 2009; Geser et al., 2010). A well known example is its role in the splicing of cystic fibrosis transmembranous conductance regulator mRNA (Buratti selleck inhibitor et al., 2001). Of interest is the finding that another target for the Epigenetic inhibitor order action of TDP-43 in mRNA processing is the protein SMN, deficiency of which results in spinomuscular atrophy, an infantile or juvenile onset motor neuron disorder (Burghes & Beattie, 2009). Overexpression of TDP-43 enhances exon 7 inclusion during SMN splicing, a crucial event in yielding fully active SMN protein (Bose et al., 2008). SMN deficiency in its turn is thought to cause spinomuscular atrophy through defective RNA processing or

transport (Burghes & Beattie, 2009). The possible link between SMN and TDP-43 is of major interest when thinking of a common pathway for motor neuron degeneration. The more than 25 mutations found in the TARDBP gene are, primarily, missense mutations and are almost exclusively located in the C-terminal (glycine-rich) part of the protein (Lagier-Tourenne & Cleveland, 2009). There is also a truncating mutation in this gene (Daoud et al., 2009). TARDBP mutations are rare: they probably account for < 5% of familial ALS, i.e. < 1% Teicoplanin of all ALS (Ticozzi et al., 2009a). The major interest in them comes from the finding mentioned above, that wildtype TDP-43 containing inclusions are found in the majority of sporadic

ALS patients (Neumann et al., 2006; Fig. 3). Here, we will refer to this abnormal form of TDP-43 as TDP-43SALS/FTLD in contrast to ‘normal’ TDP-43, reminiscent of the naming in prion disease, where PrPC refers to the normal PrP and PrPSc refers to the pathogenic form of PrP in sporadic and infectious Creutzfeldt–Jakob disease; it does not differ from normal PrPC in its amino acid sequence. Mutant TDP-43 refers to the mutant proteins causing the hereditary forms of ALS, just as with mutant PrP and Creutzfeldt–Jakob disease, and will be referred to as TDP-43mutant. An overwhelming number of papers on the role of TDP-43 in neurodegeneration have been published over the last 2 years. A common finding seems to be that TDP-43mutant and TDP-43SALS/FTLD are mislocated, hyperphosphorylated, abnormally processed and ubiquitinated.

Real-time PCR and chromatin immunoprecipitation analysis were then used to explore alterations in gene expression and modifications

LGK-974 of chromatin structure associated with the plastic outcome caused by fluoxetine in the visual system. Local infusion of 5-HT into visual cortex restored susceptibility to monocular deprivation in adulthood whereas infusion of WAY-100635, trkB-IgG or U0126 prevented the process of plasticity reactivation in fluoxetine-treated animals. Long-term fluoxetine treatment promoted a transient increase of Bdnf expression in the visual cortex, which was paralleled by an increased histone acetylation status at Bdnf promoter regions and by decreased expression of Hdac5. Accordingly, enhancing histone acetylation levels by systemic treatment with Trichostatin-A reactivated plasticity in the adult while

WAY-100635-infusion prevented epigenetic modifications in Bdnf promoter areas. The data suggest a key role for 5-HT1A receptor and BDNF-trkB signalling in driving a transitory epigenetic remodelling of chromatin structure that underlies the reactivation of plasticity in the visual system. “
“Gamma-band activity (30–90 Hz) and the synchronization of neural activity in the gamma-frequency range have been observed in different cortical and subcortical Ibrutinib nmr structures and have been associated with different cognitive functions. However, it is still unknown whether gamma-band synchronization subserves a single universal function or a diversity of functions across the full spectrum of cognitive processes. Here, we address this question reviewing the mechanisms of gamma-band oscillation generation and the functions associated with gamma-band activity across several cortical and subcortical structures. Additionally, we raise a plausible explanation of why gamma rhythms are found so ubiquitously across brain structures. Gamma band activity originates from the interplay between inhibition and excitation. We stress that gamma oscillations, associated with this interplay, originate

from basic functional motifs that conferred advantages Glutathione peroxidase for low-level system processing and multiple cognitive functions throughout evolution. We illustrate the multifunctionality of gamma-band activity by considering its role in neural systems for perception, selective attention, memory, motivation and behavioral control. We conclude that gamma-band oscillations support multiple cognitive processes, rather than a single one, which, however, can be traced back to a limited set of circuit motifs which are found universally across species and brain structures. “
“To investigate the role(s) of protein-tyrosine sulfation in the retina, we examined retinal function and structure in mice lacking tyrosylprotein sulfotransferases (TPST) 1 and 2. Tpst double knockout (DKO; Tpst1−/−/Tpst2 −/−) retinas had drastically reduced electroretinographic responses, although their photoreceptors exhibited normal responses in single cell recordings.

Percutaneous drainage may be an alternative, but only in selected patients, to preserve splenic functions. However, splenectomy remains the first line of treatment.17 Giant splenic abscess may complicate Salmonella infection, even in young immunocompetent travelers with likely preexisting splenic abnormality. Treatment always involves association of surgery (splenectomy or needle aspiration) and appropriate antibiotherapy. The authors thank Jessica Saint-Pierre for editorial assistance. The authors state that they have no conflicts of interest to declare. “
“Extensive venous thrombosis is usually seen postmortem in amebic liver abscess

because of its dismal prognosis. Herein, we describe amebic liver abscess, whose late diagnosis led to multiple deep

thromboses, PTC124 chemical structure pulmonary embolism, and right atrial thrombosis, in this patient with patent foramen ovale. A 23-year-old man, originally from Sri Lanka and living in France for 2 years, consulted in our emergency department for a 1-month history of fever and night sweats, non-productive cough, dyspnea, and involuntary weight loss of 10 kg. He had no remarkable medical history Selleck DZNeP but one of his roommates had recently been treated for tuberculosis. He was febrile (temperature 39°C), with normal blood pressure (120/80 mm Hg) and heart rate (120 beats/min). Physical examination was normal. He had no abdominal pain. Chest radiograph findings were unremarkable. Laboratory investigations showed mild hyponatremia, a leukocyte count of 18,300 cells/mm3 with 84% neutrophils. The C-reactive protein level was 274 mg/L but hepatic test results were abnormal, with liver enzyme (alkaline phosphatase and γ-glutamyltransferase) levels twofold higher than normal values. Two sets of blood cultures were negative. He was initially isolated for suspected tuberculosis and also given empirical Urease amoxicillin and erythromycin. Sputum smears were negative. Because of sustained dyspnea and fever, contrast-medium chest computed tomography scans were obtained

for suspected pulmonary embolism. Images showed a large thick-walled liver abscess (diameter 6.5 cm) located in the hepatic dome, a mild pleural effusion on the right, and inferior vena cava thrombosis (Figure 1A), and a large pulmonary embolism (Figure 1B) and right atrial thrombosis. Hepatic ultrasonography confirmed the presence of an abscess of heterogeneous, compartmentalized appearance, suggestive of a hydatid cyst. Transthoracic echocardiography confirmed the atrial thrombosis (Figure 1C) in the interatrial septum, associated with abnormal color Doppler flow, corresponding to a patent foramen ovale; systolic pulmonary artery pressure was evaluated at 38 mm Hg. The patient refused transesophageal echocardiography. Cerebral magnetic resonance imaging ordered because of recent-onset headaches was normal. Doppler ultrasonography of the lower extremities was normal and he had no underlying comorbidity predisposing to venous thrombosis.

There were no discontinuations because PF-562271 datasheet of nervous system events in the etravirine group (vs. 0.5% in the placebo group) and a very low frequency of discontinuations because of psychiatric events in both the etravirine and placebo treatment groups (0.3% and 0.2%, respectively). The frequency of grade 3 or 4 nervous system AEs of interest was low and comparable between the treatment groups, and similar proportions of patients reported grade 3 or 4 psychiatric events of interest (Table 1). By preferred term, and regardless of severity or causality, the most common nervous system events

of interest were headache, dizziness and somnolence, and the most common psychiatric events of interest were depression, insomnia and anxiety, each of which occurred in the etravirine

group at a rate similar to that in the placebo group (Table 1). Most neuropsychiatric events of interest occurred early during treatment (Fig. 1). A previous history of psychiatric disorders was found to increase the occurrence of nervous Akt inhibitor system and psychiatric AEs of interest in both treatment groups (P < 0.0001 and 0.0728 in the etravirine and placebo groups, respectively). Of those patients with a psychiatric history [46.7% (n = 280) and 43.9% (n = 265) in the etravirine and placebo groups, respectively], the overall frequency of neuropsychiatric events of interest was 42.1% and 40.0% in the etravirine and placebo groups, respectively; in patients with no psychiatric history, the corresponding frequencies were 26.3% and 32.7%, respectively. Regardless of severity or causality and consistent with previous findings at weeks 24 and 48, rash occurred at a significantly higher frequency

in the etravirine arm than in the placebo arm (20.5% vs. 11.8%, respectively; 95% CI 4.6–12.9; P < 0.0001, Fisher's exact test; predefined analysis) (Table 2). Most cases of rash occurred within the first 2 weeks of treatment and resolved with continued treatment; the frequency of rash occurring after 48 weeks was low. Discontinuation selleck chemicals llc because of rash was infrequent in the etravirine group (2.2%, all of which occurred in the first 48 weeks of treatment) and there were no discontinuations because of rash in the placebo group. The majority of rash events were grade 1 or 2 in severity (Table 2). One patient in the placebo group developed a grade 4 vesicular rash in the first 48 weeks (Stevens–Johnson syndrome), thought to be related to an allergic reaction to trimethoprim/sulfamethoxazole; no other grade 4 rashes were reported. There were no clear differences between the treatment groups for different individual types of rash apart from general rash (Table 2). A significantly higher proportion of women than men in the etravirine group reported rash [31.7% (n = 19) vs. 19.3% (n = 104), respectively; P = 0.

Although a very small number of Daporinad purchase non-Purkinje cells were sometimes EGFP-positive, they were always negative for DsRed2 (Fig. 3D, a–c). The only DsRed2

signals observed outside the cerebellum were within the dorsal cochlear nucleus (Fig. 3D, d). Indeed, cartwheel cells in the dorsal cochlear nucleus are known to share several cell markers, such as calbindin and L7, with Purkinje cells, and cartwheel and Purkinje cells are probably derived from common precursors (Berrebi et al., 1990). Together, these results indicate that IUE can drive the expression of exogenous genes specifically in Purkinje cells in a temporally controlled manner, by using the L7 promoter and inducible Cre/loxP system. As shown by the successful application of an inducible Cre/loxP system consisting of three plasmids (Fig. 3A), a major advantage of the gene delivery by in vivo electroporation is that

multiple and very large genes can be coexpressed with high efficiency (Saito & Nakatsuji, 2001; Matsuda & Cepko, 2007; Barnabe-Heider et al., 2008). To further confirm this principle in our system, we electroporated at E11.5 three plasmids encoding three different fluorescent proteins: mito-ECFP, which is designed to localize to mitochondria, EGFP-β-actin (Furuyashiki et al., 2002) and DsRed2. The confocal z-stack images of spectral data were obtained on Forskolin mouse fixed sagittal sections at P14, and the individual ECFP, EGFP and DsRed2 fluorescence images were separated by the linear unmixing method (Zimmermann et al., 2003). Most Thiamet G labeled Purkinje cells (99.1%; 445 of 449 cells) expressed all three fluorescent proteins (Fig. 4).

The DsRed2 signals were observed diffusely throughout Purkinje cells, including the soma, dendrites, spines and axons. In contrast, the EGFP-β-actin signals accumulated in the dendritic spines and nuclei, while the mito-ECFP signals were observed in the soma and dendritic shafts. Next, to examine whether a large gene can be introduced into Purkinje cells by IUE, we used cDNA encoding Bassoon, a large protein selectively localized at the active zone of presynaptic nerve terminals (tom Dieck et al., 1998). We electroporated a plasmid (approximately 17 kb) encoding mouse Bassoon fused to mCherry (mCherry-Bassoon; approximately 12.5 kb) and a plasmid encoding EGFP at E11.5. Confocal imaging of fixed cerebellum at P14 revealed punctate mCherry-Bassoon signals along EGFP-positive Purkinje cell axons (Fig. S4). In addition, mCherry-Bassoon signals were colocalized with immunoreactivity for vesicular GABA transporter (VGAT), a presynaptic marker (Fig. S4). Together, these results illustrate that an advantage of IUE-based gene delivery into Purkinje cells is that not only can multiple genes be coexpressed, but also that large genes can be transfected with high efficiency.

L.C.O. developed the analysis plan and performed all the statistical evaluations and models. B.G., R.I.M. and J.P. developed the instruments for data collection and the study database. J.S.M., J.S., B.C., O.G.M. and M.B.L. contributed to data collection and verification. W.H.B., L.C.O., M.H.L., A.L.R. and B.G. contributed to the process of writing the manuscript. J.S.M., J.S., M.B.L. and O.G.M. participated in the correction of the final version of the manuscript. “
“Chronic kidney

disease (CKD) is common in HIV-infected individuals, and is associated with mortality in both the HIV-infected and general populations. Urinary markers of tubular injury have been associated with future kidney disease risk, but associations with mortality are unknown. Selleck PF 2341066 We evaluated the associations of urinary interleukin-18 (IL-18), liver fatty acid binding protein

(L-FABP), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL) and the albumin-to-creatinine ratio (ACR) with 10-year, all-cause death in 908 HIV-infected women. Serum cystatin C was used to estimate the glomerular filtration rate (eGFRcys). There were 201 deaths during 9269 person-years of follow-up. After demographic adjustment, compared with the lowest tertile, the highest tertiles of IL-18 [hazard ratio (HR) 2.54; 95% confidence interval (CI) 1.75–3.68], KIM-1 (HR 2.04; 95% CI 1.44–2.89), NGAL (HR 1.50; 95% CI 1.05–2.14) and ACR (HR 1.63; 95% CI 1.13–2.36) were associated with buy Everolimus higher mortality. After multivariable adjustment including adjustment for eGFRcys, only the highest tertiles of IL-18 (HR 1.88; 95% CI 1.29–2.74) and ACR (HR 1.46; 95% CI 1.01–2.12) remained independently associated with mortality. Findings for KIM-1 were borderline (HR 1.41; 95% CI 0.99–2.02). We found a J-shaped association between L-FABP and mortality. Compared with persons in

the lowest tertile, the HR for the middle tertile of L-FABP was 0.67 (95% CI 0.46–0.98) after adjustment. Associations were stronger when IL-18, ACR and L-FABP were simultaneously included in models. Among HIV-infected Sclareol women, some urinary markers of tubular injury are associated with mortality risk, independently of eGFRcys and ACR. These markers represent potential tools with which to identify early kidney injury in persons with HIV infection. “
“Improvements in neurocognitive (NC) function have been associated with commencing antiretroviral therapy in HIV-infected subjects. However, the dynamics of such improvements are poorly understood. We assessed changes in NC function via a validated computerized battery (CogState™, Melbourne, Victoria, Australia) at baseline and after 24 and 48 weeks in a subset of therapy-naïve neuro-asymptomatic HIV-infected subjects, randomized to commence three different antiretroviral regimens.

L.C.O. developed the analysis plan and performed all the statistical evaluations and models. B.G., R.I.M. and J.P. developed the instruments for data collection and the study database. J.S.M., J.S., B.C., O.G.M. and M.B.L. contributed to data collection and verification. W.H.B., L.C.O., M.H.L., A.L.R. and B.G. contributed to the process of writing the manuscript. J.S.M., J.S., M.B.L. and O.G.M. participated in the correction of the final version of the manuscript. “
“Chronic kidney

disease (CKD) is common in HIV-infected individuals, and is associated with mortality in both the HIV-infected and general populations. Urinary markers of tubular injury have been associated with future kidney disease risk, but associations with mortality are unknown. click here We evaluated the associations of urinary interleukin-18 (IL-18), liver fatty acid binding protein

(L-FABP), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL) and the albumin-to-creatinine ratio (ACR) with 10-year, all-cause death in 908 HIV-infected women. Serum cystatin C was used to estimate the glomerular filtration rate (eGFRcys). There were 201 deaths during 9269 person-years of follow-up. After demographic adjustment, compared with the lowest tertile, the highest tertiles of IL-18 [hazard ratio (HR) 2.54; 95% confidence interval (CI) 1.75–3.68], KIM-1 (HR 2.04; 95% CI 1.44–2.89), NGAL (HR 1.50; 95% CI 1.05–2.14) and ACR (HR 1.63; 95% CI 1.13–2.36) were associated with RG7422 in vivo higher mortality. After multivariable adjustment including adjustment for eGFRcys, only the highest tertiles of IL-18 (HR 1.88; 95% CI 1.29–2.74) and ACR (HR 1.46; 95% CI 1.01–2.12) remained independently associated with mortality. Findings for KIM-1 were borderline (HR 1.41; 95% CI 0.99–2.02). We found a J-shaped association between L-FABP and mortality. Compared with persons in

the lowest tertile, the HR for the middle tertile of L-FABP was 0.67 (95% CI 0.46–0.98) after adjustment. Associations were stronger when IL-18, ACR and L-FABP were simultaneously included in models. Among HIV-infected Amylase women, some urinary markers of tubular injury are associated with mortality risk, independently of eGFRcys and ACR. These markers represent potential tools with which to identify early kidney injury in persons with HIV infection. “
“Improvements in neurocognitive (NC) function have been associated with commencing antiretroviral therapy in HIV-infected subjects. However, the dynamics of such improvements are poorly understood. We assessed changes in NC function via a validated computerized battery (CogState™, Melbourne, Victoria, Australia) at baseline and after 24 and 48 weeks in a subset of therapy-naïve neuro-asymptomatic HIV-infected subjects, randomized to commence three different antiretroviral regimens.

On the other hand, when pBL21 was introduced into the Δpmt mutant IB25, mycelium could only be grown under noninducing conditions (i.e. in the absence of thiostrepton) where no complementation of the Δpmt mutation was observed (Fig. S4); adding thiostrepton to the medium resulted in a lack of growth, either in liquid medium or on solid medium, meaning that expression of this chimeric Pmt protein was lethal (Fig. S6). Therefore, replacement of the N-terminal region containing the first extracellular loop of PmtMtu by that of PmtSco was apparently not innocuous. One possibility is that this construct results

in a misfolded protein that is toxic; we consider this unlikely, given the structural conservation shown by both Pmt proteins (Fig. S5). Another possible explanation is that the lethal phenotype is the result of a nonproductive interaction between selleck the chimeric Pmt and the Sec translocon, perhaps affecting Sec function to such an extent as to make it nonfunctional. We attempted to show specific interactions between components of the S. coelicolor Sec translocon and either PmtSco or PmtMtu using the bacterial two-hybrid system of Buparlisib chemical structure Karimova et al. (1998), but no significant interactions could be observed (data not shown).

It has also been recently suggested that interaction between corynebacterial Pmt and Lnt might be essential for Pmt function in these bacteria, as there was no detectable glycosylation of a lipoprotein that is normally glycosylated in the absence of Lnt (Mohiman et al., 2012). Mycobacteria are closely related to corynebacteria, so it find more is conceivable that PmtMtu is not functional in S. coelicolor because it is unable to interact with S. coelicolor Lnt1. Because our results show that Lnt1 is not required for PmtSco function, this might reveal a fundamental difference between these two bacterial groups. Because PmtMtu failed to complement the Δpmt deletion of S. coelicolor in vivo, we wondered

whether Pmt activity could be detected in vitro, using the assay previously described for glycosylation of the synthetic A3 peptide derived from the Apa protein with a purified membrane fraction (Cooper et al., 2002). As can be seen in Fig. S7, membranes of wild-type S. coelicolor J1928 were able to mannosylate the A3 peptide, whereas those of the Δpmt mutant IB25 were not. When plasmid pBL12 encoding PmtSco was introduced into the Δpmt strain IB25 in vitro activity was restored, but no Pmt activity was detected when pBL9 (encoding PmtMtu) was introduced into this strain, meaning that this enzyme is not functional when expressed in S. coelicolor. This result supports the idea that PmtMtu is not capable of forming a productive interaction with the S.

For routine monitoring purposes, viral load testing should be performed on plasma. The viral load assays can be adapted to perform well in other compartments including cerebrospinal PLX3397 manufacturer fluid (CSF) and seminal plasma. However, routine monitoring of viral load in compartments other than plasma is not currently recommended because of undemonstrated clinical utility or practicality (IV). Testing of CSF collected from patients with neurological

disease should be considered, especially in patients with suppressed plasma viral load (III). Using sensitive testing methods in research settings, HIV-1 RNA can be detected in plasma in a large proportion of patients receiving standard ART regimens and showing a viral load stably below 50 copies/mL for many years [1-10]. This residual viraemia is not generally associated with the emergence of drug resistance or low antiretroviral drug levels in plasma [8, 11, 12], and is not responsive to short-term intensification with efavirenz, ritonavir-boosted atazanavir, ritonavir-boosted lopinavir, enfuvirtide or raltegravir

this website [8-10]. These findings are shedding new light on the significance of low-level viraemia detected by routine viral load assays during ART, while falling short of providing clear guidance for its management in patients receiving standard ART regimens. As a consequence of technical fluctuation around the cut-off level of quantification, routine viral load assays are more likely to report low-level viraemia above 50 copies/mL in treated patients who have a level of residual viraemia just below the assay cut-off (e.g. around 30 copies/mL), as seen in some patients [8]. The detection of this residual viraemia is likely to be technically inconsistent, leading to the phenomenon of viral load ‘blips’. Viral load ‘blips’ are defined as transient rises in viral load to levels above the lower detectable limit of the assay [13]. Although currently there

is no consensus definition, in practice a blip is considered to be a single viral load measurement of 50–1000 copies/mL preceded Farnesyltransferase and followed by a measurement of fewer than 50 copies/mL. It is controversial whether blips are associated with an increased risk of virological failure, although most studies show that isolated blips are of little clinical significance [14-17]. The scenario is different, however, for patients with two or more consecutive measurements above 50 copies/mL [17] and possibly for patients with frequent blips, as these are more likely to experience virological rebound above 400 copies/mL. These patients may benefit from intervention to review expected drug potency, adherence and tolerability, and drug resistance, and modifications of therapy should be considered in line with treatment guidelines [18].

[4] The EU project ShipSan documented the high diversity of practices, administrative arrangements, qualifications, staffing, and equipment of competent port health authorities among EU countries.[5] Clearly it will need a thorough assessment of existing infrastructures and a political commitment to close the gaps and allocate resources. Hopefully, the two main evils that hamper effective public health services in many ports will not be overlooked by countries:

corruption and lack of protection of personal health data. As long as ships’ crews experience intimidation and arbitrariness in global ports, compliance and trustful cooperation of ship personnel AZD5363 price with the public health services will be impaired and opportunities for interventions missed. This issue of the Journal of Travel Medicine includes two papers that pose a timely reminder to the events that must be considered when allocating

public health capacities to serve ships and ports: Elaine Cramer and colleagues[6] summarize reports to the electronic Maritime Illness and Death Reporting System of the Centers of Disease Control from 2005 to 2010. Varicella was the vaccine-preventable disease most frequently reported to CDC by cruise ships. It must be of interest to contingency planning of shipping companies and health authorities alike that 70% of reported cases were associated with outbreaks on board. The number of cases per outbreak ranged between 2 to 9 with a majority of first-generation NVP-BGJ398 mouse cases and a substantial number of two- or more generation cases. In the opinion of Elaine Cramer and co-authors the CDC protocol for varicella outbreaks on cruise ships[7] was useful to rapidly curtail respective outbreaks. This is important information not only to cruise ships but also to cargo ships where often less than 30 seafarers, many of South East Asian origin are responsible for the ship’s safe navigation. Port health services are better being ready to assess immunity and offer post-exposure vaccination

to ships’ non-immune crew and to passengers. Mirtuka and colleagues[8] describe the enormous consequences Aspartate of reporting two crew patients, one from Ukraine and one from the Philippines, with rashes after signing to a cruise ship in 2006. The comprehensive investigations over 36 days revealed 1 case of rubella, 3 cases of measles and 11 cases of varicella. A stunning 30,000 passengers, traveling on this ship were notified of potential exposures to measles and rubella with no cases detected among passengers. All 1,197 crew members were considered potential contacts, assessed for immunity to measles and rubella and underwent active and passive surveillance for rash illness. The total costs were estimated at $67,000 for vaccinations, supplies, and health department staff time. Only three of the crew had sufficient immunization records to prove immunity.