The cerebellum has served as an important system for studying neurodevelopment and information processing because of its well-characterized circuits, which consist of relatively few cell types (Altman & Bayer, 1997). Cerebellar Purkinje cells have been prominently featured in these studies. For example, the long-term depression (LTD) of synaptic transmission at parallel fiber (PF)–Purkinje cell synapses

is thought to underlie certain forms of motor learning in the cerebellum (Ito, 1989). Furthermore, the unique shape of Purkinje cell dendrites makes them especially useful for investigating the molecular mechanisms underlying neuronal dendrite development (Sotelo & Dusart, 2009). Therefore, various methods have been developed to molecularly perturb Purkinje cells by expressing exogenous genes. Although Purkinje www.selleckchem.com/products/dinaciclib-sch727965.html cells can be transgenically targeted by using the L7 (Pcp2) promoter (Oberdick et al., 1990; Smeyne et al., 1991; Tomomura et al., 2001), the selection of mouse lines expressing high levels of transgenes can be time-consuming and labor-intensive (Yuzaki, 2005). Furthermore, the L7 promoter turns on relatively late in

postnatal development (Smeyne et al., 1991; Tomomura et al., 2001), making it difficult for researchers to perturb early developmental events. As an alternative approach, viral vectors, including adenovirus (Hashimoto et al., 1996), adeno-associated virus (AAV) (Kaemmerer et al., 2000), herpes simplex virus Linsitinib in vitro (Agudo et al., 2002), Sindbis virus (Kohda et al., 2007) and lentivirus (Torashima et al., 2006), have been used to express molecules in Purkinje cells in vivo. However, each vector has certain drawbacks. For example, approximately 30% of the cells infected by one of the best Purkinje cell-specific lentiviral vectors are non-Purkinje cells

(Takayama et al., 2008). In addition, it takes several days to weeks for AAV and lentiviral vectors to maximally express foreign genes. Finally, it is often difficult to express large and multiple genes in Purkinje cells with viral Adenosine vectors. Therefore, a method that can complement the current transgenic and viral vector approaches is desired. In utero electroporation (IUE), in which electrical pulses are applied through the uterine wall, has recently emerged as a useful method for transferring genes into restricted types of neuronal precursors in vivo (Saito & Nakatsuji, 2001; Tabata & Nakajima, 2001). An advantage of IUE is that large and multiple genes can be introduced into neurons during very early developmental periods (De Vry et al., 2010). Furthermore, by using cell-type-specific and/or inducible promoters, foreign genes can be expressed in a particular neuronal subset within a distinct time frame (Kolk et al., 2011). Although IUE has been successfully applied to various neurons in the cerebral cortex (Saito & Nakatsuji, 2001; Tabata & Nakajima, 2001), hippocampus (Navarro-Quiroga et al., 2007), thalamus (Bonnin et al.

In their study, young children had higher proportionate morbidity rates.4 Newman-Klee and colleagues stated that the similar incidence of morbidity in children and adults, as well as the mildness of the morbid episodes, challenges the view that it is unwise to travel with small children.5 We initiated a prospective study which aimed at (1) assessing the incidence rate of ailments in children and their parents or caregivers, further referred to as parents, traveling to (sub)tropical destinations, and (2) characterizing the types of ailments occurring and defining risk

factors for traveling children in comparison to their parents. This prospective observational study was conducted at the Travel Clinic Sirolimus mouse of the Havenziekenhuis in Rotterdam, the Netherlands, from May to August 2010. Ethical clearance was granted by the ethics committee of the Erasmus Medical Centre, Rotterdam. Participants were included after written informed consent. Families visiting the Travel Clinic for pre-travel health advice and expat families receiving a medical checkup were eligible for inclusion. The inability to read and write in Dutch was considered an exclusion criterion. All participants received a standardized questionnaire, detailing 33 defined ailments.6 The forms were filled out prior to departure and weekly during their stay abroad. A parent filled out the questionnaires

of children with an age below 12 years. Participants who failed to return or complete their questionnaires were considered lost to follow-up. Ailments were graded semi-quantitatively as follows: Grade Arachidonate 15-lipoxygenase I (mild): In cases where an ailment did not affect daily routine. The ailment rates were expressed

click here as the number of ailments per personmonth of travel. Given the broad array of destinations, destinations were grouped by continent in Asia, Africa, and South and Central America (S/C America). Turkey was regarded as an Asian country. To evaluate ailments rate in relation to a specific destination, ailments were also grouped in dermatological disorders, respiratory disorders, diarrheal disorders, and systemic febrile illnesses. Statistical analysis was performed with GraphPad Prism software, version 5.03 (GraphPad software, Inc., San Diego, CA, USA). The Log-rank (Mantel–Cox) test was used for comparison of Kaplan–Meier survival curves. Ailment rates between the various age categories were compared with the Kruskal–Wallis (non-parametric ANOVA) test followed by Dunn’s multiple comparisons test. Relative risks were calculated using the Fisher’s exact test using Yate’s continuity correction. Of the 233 children and 104 parents participating, we excluded 12 children and 7 parents who changed their travel plans, traveled to a European country, or traveled after September 2010, leaving 221 children and 97 parents. In total 152 children (69%) and 47 parents (48%) returned their questionnaires. The general characteristics and travel demographics are shown in Table 1.

Similar to other studies, overweight, obesity, increasing

TG and hyperglycaemia were significantly associated with an increased risk for elevated ALT. These conditions are significant risk factors for nonalcoholic fatty liver disease and nonalcoholic steato-hepatitis (NASH), which these elevations in ALT could represent [7, 13-15]. NASH or fatty liver, associated with metabolic syndrome, diabetes mellitus and hypertriglyceridaemia have been reported to be the cause of the abnormal liver enzymes in HIV-infected patients in several recent studies [14, 15]. In contrast to other studies, we found a reduced risk of elevated ALT with LDL cholesterol > 130 mg/dL [13-15]. Although nonfasting measurement of lipids may have led to this contradictory finding, the relationship between LDL cholesterol and elevated ALT in ART-naïve HIV-infected this website DZNeP patients is still unclear and deserves further investigation in the absence of ART exposure. In this study, we noted an interesting gender difference with respect to the risk of elevated ALT. Compared with nonpregnant women, men had an increased risk of ALT > 40 IU/L, while pregnant women had a reduced risk of elevated ALT in adjusted analyses.

This gender discrepancy is similar to a finding by Weidle et al., who observed men to have a 55% higher risk of elevated baseline liver enzymes than their female counterparts [8]. The reasons for this gender discrepancy are not clear. One potential confounder that was not examined in our study and could have contributed to the excess risk of ALT elevation is alcohol consumption, which has been shown to be significantly higher in men compared

with women in urban Tanzanian settings [24]. Interestingly, pregnant HIV-infected patients were at a reduced risk for elevated baseline PIK3C2G ALT compared with nonpregnant women. There have been contradictory reports demonstrating the risk of elevated liver enzymes among pregnant HIV-infected women exposed to ART, particularly nevirapine [22-24]. There are no data, however, to suggest that the same risk applies to pregnant women in the absence of ART [25] and this therefore deserves further study. However, physiological changes during a normal pregnancy have been associated with lower than normal liver enzymes, including ALT [26]. Surprisingly, we found a reduced risk for elevated ALT among HIV-infected patients who were on anti-TB therapy at the time of recruitment to HIV clinics. Few data exist on hepatotoxicity of TB drugs among HIV-infected patients prior to ART initiation. Two studies by Hoffman and Weidle et al. documented an increased risk of hepatotoxicity in patients on concomitant ART and anti-TB drugs [7, 8]. Similarly, Coca et al.

Our cases provide a compelling argument for the promotion of vaccination against this disease, as recommended by the World Health Organization. The authors state they have no conflicts of interest to declare. “
“The aim of this prospective observational cohort study was to investigate relationships

between acute mountain sickness (AMS) and physical and mental health during a high altitude expedition. Forty-four participants (mean age, 34 ± 13 y; body mass index, 23.6 ± 3.5 kg·m2; 57% male) completed the Dhaulagiri base camp trek in Nepal, a 19-day expedition attaining 5,372 m. Participants self-reported the following daily physical and mental health: AMS (defined by Lake Louise diagnosis and individual and total symptom scores), upper respiratory symptoms, diarrhea, and anxiety, plus physiological and behavioral AZD2281 in vitro factors. The rate of Lake Louise-defined AMS per 100 person days was 9.2 (95% CI: 7.2–11.7). All investigated illnesses except diarrhea increased with altitude (all p < 0.001 by analysis of variance). Total AMS symptom score was associated with a lower arterial oxygen saturation, higher resting heart rate, more upper respiratory and diarrhea symptoms, greater anxiety, and lower fluid intake (all p < 0.02 by longitudinal multiple regression

analyses). However, only upper respiratory symptoms, Veliparib heart rate, arterial oxygen saturation, and fluid intake predicted future AMS symptoms [eg, an increase in upper respiratory symptoms by 5 units predicted an increase in the following day's AMS total symptom score by 0.72 units (0.54–0.89)]. Upper respiratory symptoms and anxiety increasingly contributed to symptom burden as altitude was gained. Data were consistent with increased heart rate, decreased arterial oxygen saturation, reduced fluid intake, and upper respiratory MTMR9 symptoms being causally associated with AMS. Upper respiratory symptoms and fluid

intake are the simplest targets for intervention to reduce AMS during high altitude exposure. Many people travel to mountainous regions for work and recreation. In Nepal alone, over 130,000 foreigners visit each year to complete trekking and mountaineering activities[1] of which half may get acute mountain sickness (AMS).[2] However, general illnesses such as diarrhea and upper respiratory symptoms, and also psychological disturbances, contribute to ill health experienced at altitude.[3-5] The intrusive nature of such general illnesses is likely to limit work capacity and enjoyment. There is also a substantial risk of having to be evacuated from expeditions due to such illnesses,[6] and a small but real risk of such illnesses eventually resulting in death.[7] Furthermore, conditions such as diarrhea, upper respiratory symptoms, and anxiety may be of considerable relevance to AMS since the conditions share many of the same symptoms (eg, nausea).

13 Data from annual surveys do not, however, reflect these episodes. The numbers of travelers to malaria-endemic countries have increased since 2000 and were highest

in the first and last quarter of the year, probably reflecting Christmas and winter holidays. The number of malaria cases did not follow any seasonality, likely because of the small number of cases per quarter. The lack of increase in the numbers of organized 17-AAG order trips and the concomitant increase in traveling to malaria-endemic areas suggest that self-organized trips to malaria-endemic areas has increased. We used antimalarial drug sales as an indicator of the use of chemoprophylaxis. Drug sales have also been used as an indirect measure of disease activity.14 Antimalarial drug sales were highest in the first and last quarter of the years, following the same trend as traveling to malaria-endemic countries. Drug sales see more decreased since 1997, but started to increase slowly from 2005 onward. This increase coincided with the marketing authorization of atovaquone/proguanil combination in Finland in 2006. The drug got its first marketing approval in 1996, but was registered only 10 years later. Sales of proguanil decreased until 2006 when it stopped being used as a single agent. During

the 1990s chloroquine was used also to treat rheumatic disorders but, in the last 10 years, its use for this purpose was very unlikely (Professor Marjatta Leirisalo-Repo, personal communication, January 25, 2010). This change probably contributes to the decrease in the use of chloroquine. Caution Dapagliflozin should be used when interpreting the trends on DDD sales. Differences in drug accessibility and approval schemes should be taken into account when drug usage is compared between countries. Although doxycycline is included in the Finnish guidelines for malaria chemoprophylaxis, it was not included in our study. Doxycycline is mainly

used for other indications, and there was no way of discriminating between the proportions of sales used for different purposes. Taking this into account, it remains fully possible that the use of doxycycline as an antimalarial could have increased significantly and this increase could, at least partly, account for the decrease observed with the other drugs sales. Our results show that antimalarial drug sales cannot be used alone to assess the use of chemoprophylaxis. The decrease in drug sales may be explained by several factors such as travelers fearing adverse drug reactions,15 choosing to buy drugs at destination,16 or underestimating the risk of malaria. During recent years internet discussion sites have become an important source of information for travelers and may sometimes even be trusted more than official sites. In addition, the level of compliance to antimalarials is known to be low,5,6,17 and no data exist as to whether people buying the drugs actually take them accurately.

Furthermore, Tn5251-like elements are highly capable of capturing other genetic elements carrying different antibiotic resistance determinants such as the mef(E) and erm genes conferring macrolide resistance, aadE, sat4 and aphA-3 conferring resistance to streptomycin, streptothricin and kanamycin, respectively. These features make these elements successful in disseminating multidrug resistance determinants among pathogenic bacterial species. In this context, characterization

of Tn5251 contributes to the understanding of the selleck chemicals llc mechanisms of the spread of antibiotic resistance. This study was supported by the European Commission grants ANTIRESDEV HEALTH-F3-2009-241446 and by Universita’ degli CHIR-99021 Studi di Siena (PAR). “
“In a growth-restricting environment, mutants arise that are able to take over bacterial populations by a process known as adaptive mutation or stationary-phase mutation. This process is best studied in Escherichia coli. The genus Pseudomonas represents one of the largest groups of bacteria able to colonize multiple habitats and to adapt rapidly to new environments. The majority of bacteria including pseudomonads contain a different set of DNA polymerases and DNA repair enzymes

than those identified in E. coli. The aim of this review is to provide an overview of the results of studies of mutagenic processes in pseudomonads and to discuss these results in the light of the mechanisms of stationary-phase mutagenesis discovered in E. coli. Conditions for unrestricted growth are rarely met in natural environments, and therefore, most bacteria are in a state of slow or nongrowth, also called as a stationary phase (Poulsen et Oxymatrine al., 1995; Bååth, 1998). Under stressful, growth-restricting conditions (e.g. nutrient starvation, during colonization of the host organism), microbial populations can rapidly evolve. Genetic changes in microbial populations can occur fast through the acquisition and incorporation of foreign DNA or through mutation. Genetic changes that result from the introduction of mutations

into DNA can arise by various mechanisms, including those caused by DNA damage, and via errors introduced during DNA replication. Replication errors can result from the failure of base selection, proofreading and DNA mismatch repair (MMR), which act sequentially to ensure the fidelity of replication (Schaaper, 1993). Mutagenesis occurring in growth-restricted cells is called adaptive mutation or stationary-phase mutation (Foster, 1999; Rosenberg, 2001). It has been suggested that a variety of environmental stresses induce genomic change in bacteria, generating occasional fitter mutants and potentially accelerating the evolution of bacterial populations (Metzgar & Wills, 2000; Rosenberg, 2001; Tenaillon et al., 2001; Bjedov et al., 2003; Kivisaar, 2003; Miller, 2005; Foster, 2007; Galhardo et al., 2007; Robleto et al., 2007; Baquero, 2009).

26 Carlsten showed a protective effect of 250 mg bid but not of 125 mg bid in La Paz (3,630 m) in travelers who flew in from Miami (sea level).27 It is possible that a low dose of acetazolamide works better in partially acclimatized travelers at very high altitude than in travelers who just arrived at high altitude. Although most experts today advise a preventive dose of 125 mg twice daily, a review on efficacy of pharmacological prevention of AMS (which is not generally accepted) concluded that a daily dose of 500 mg acetazolamide was not effective while 750 mg was; and in his 2008

review, Wright concluded that 500 mg/d should be used preventively.28,29 The fact that we found no association between acetazolamide treatment and the duration of AMS may be because of the low average dose of 375 mg/d or 5 mg/kg/d that was taken, as the only (small) randomized controlled trial on efficacy of this website acetazolamide treatment used 500 mg/d, which corresponds to 7 mg/kg/d for a 70 kg person.30 It could also be explained by a difference in severity of complaints in both groups, as those who did not take acetazolamide often reported that they refrained from the treatment because the symptoms were mild. This indicates a serious bias and it implies that no conclusion regarding the effect of acetazolamide treatment on the duration of symptoms can be made. This survey has several possible weaknesses. It relies on the accuracy of

self-reported data FK228 concentration collected a few weeks after return and the assumption that the responders are representative of the target population. Chlormezanone The response rate was higher than in several other surveys on AMS4 and of the returned questionnaires, very few had missing data. We did not phone non-responders, but several of them informed us that they ended up not climbing above 2,000 m. In this study, we did not differentiate between mild and serious complaints, which implies that we cannot conclude anything on the effect of acetazolamide treatment on the duration of AMS complaints. Of course, our study is not randomized

double-blind placebo controlled, but even in the subgroup of travelers with previous AMS we found no relation between acetazolamide prevention and AMS incidence while there was no difference in risk factors like sex, age, maximum altitude, and nights of acclimatization in those who took prevention and those who did not. As most other predictors of AMS are fixed when clients come to our travel clinic, we should stress the importance of at least 2 days of acclimatization between 1,500 and 2,500 m. As Alan J. Magill explained in the Expert Opinion Series of the International Society of Travel Medicine, even those who fly to an airport at high altitude often can descend after arrival to spend a few nights at a lower altitude.31 We should also stress the importance of a flexible travel itinerary in order to be able to change it when problems arise.

Then, cells were incubated with FITC-conjugated anti-rabbit IgG 1 : 50 for 1 h at 37 °C. Fluorescence at 525 nm was measured in a microplate reader Spectramax M2e (Molecular Devices, Sunnyvale). Conidia macerated with liquid nitrogen were used as a sample of the total (extra- and intracellular) GAPDH protein. Conidia without

an immunolabeling treatment were used as the negative control. Conidial suspensions of a wild-type (WT) green fluorescent protein expressing M. anisopliae (2 × 107 conidia mL−1) were used to treat insect wings by immersion for 20 s. The wings Trichostatin A in vitro from Dysdercus peruvianus disinfected previously in 37% H2O2 were placed on the surface of 0.7% water agar and incubated for 8 h at 28 °C to induce conidial swelling and germination. The conidia were counted in five objective fields under a fluorescence microscope and recorded with three replicates of wings. The conidia were counted before learn more and after washing in 0.05% Tween 20 for 30 s. The following treatments were performed: (1) before immersion of the wings in the conidial suspension – preincubation with bovine serum albumin (BSA) (25 μg mL−1) for 1 h at 37 °C and preincubation with recombinant

GAPDH (25 μg mL−1; from M. anisopliae, Supporting Information, Appendix S1) for 1 h at 37 °C; (2) conidial suspension was treated before immersion of the wings – with anti-CHI2 antisera (1 : 100) for 1 h at 37 °C and anti-GAPDH antiserum (1 : 100, produced with P. brasiliensis GAPDH). Experiments were in triplicate; the means and SEs were determined. Statistical analysis was performed using a t-test. P values of 0.0001 or less were considered statistically significant. The ORF from gpdh1 (GenBank accession number EF050456) predicts a 338 amino acid protein with an estimated MW of 36 kDa and http://www.selleck.co.jp/products/Adrucil(Fluorouracil).html a theoretical pI of 8.26. In silico protein domain analysis found no domain other than the expected NAD-binding domain (from Val4 to Cys151) and the C-terminal domain (from Leu156 to Tyr313) typical of GAPDH (Figs 1 and S1; Appendix S2). The putative M. anisopliae GAPDH sequence

had high identity and similarity values with fungal counterparts (Table S1), and a phylogenetic tree was built (Fig. S2) showing a distribution consistent with other orthologs and one intron at a conserved position (Ridder & Osiewacz, 1992; Templeton et al., 1992; Jungehulsing et al., 1994). The M. anisopliae gpdh1 gene is a single copy (Fig. 1a). To characterize possible isoforms of the GAPDH in M. anisopliae, cell extracts were analyzed by 2-D gel electrophoresis [Fig. 1b (A)]. The immunodetection of native GAPDH isoforms was performed using anti-GAPDH P. brasiliensis polyclonal antiserum. The Western blot revealed three reactive isoforms, with pIs of 6.6, 6.8 and 7.0 [Fig. 1b (B)]. A protein with a molecular mass of 36 kDa and pI 7.0 was excised from 2-D gel electrophoresis blots of M. anisopliae mycelial protein extracts.

These phage proteins assemble stable, nonspecific pores in the bacterial envelope, allowing phage-encoded lysins (endolysins) to access their substrate (peptidoglycan) (Young & Bläsi, 1995; Wang et al., 2000). Several holin-like proteins are encoded in bacterial genomes including Gram-positive such as Staphylococcus aureus and Bacillus spp. (Loessner et al., 1999; Real et al.,

2005; Anthony et al., 2010), which display a regulatory role in the activity of murein hydrolases, autolysis and spore morphogenesis (Rice & Bayles, 2003). In the Gram-negative bacteria Borrelia burgdorferi, BlyA exhibits a holin-like function promoting the endolysin-dependent lysis and enhancing haemolytic phenotype in animal erythrocytes (Guina & Oliver, 1997; Damman et al., 2000). In addition, Escherichia coli and Salmonella spp. genomes contain GSK126 in vitro holin-like genes, but little is known about their function.

click here In this work, we performed a combination of bioinformatic, genetic and biochemical experiments in order to characterize the STY1365 small ORF of S. Typhi. Bacterial strains and plasmids used in this study are listed in Table 1. Cells were routinely grown in 2 mL Luria–Bertani (LB) broth at 37 °C with shaking. When required, media were supplemented with ampicillin (100 μg mL−1), chloramphenicol (20 μg mL−1), kanamycin (50 μg mL−1) and l-arabinose (2 μg μL−1). Solid media were prepared by addition of 1.5 g w/v agar. The nucleotide sequence from S. Typhi CT18 genome (AL513382) was accessed via the National Center for Biotechnology Information (NCBI) Genome database (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=genome) Rucaparib molecular weight and was used to compare STY1365 and both flanking regions with S. Typhimurium DT104

prophage-like element (AB104436, Saitoh et al., 2005). The STY1365 coding sequence of S. Typhi STH2370 strain was sequenced previously and it was shown to be identical to the corresponding genomic region of S. Typhi CT18 (Rodas et al., 2010). Transmembrane domains of STY1365 were analyzed using tmhmm server v2.0 program (http://www.cbs.dtu.dk/services/TMHMM-2.0/). Analysis of STY1365 predicted amino acid sequence (NC_003198.1) was performed using psi-blast program (http://www.ncbi.nlm.nih.gov/BLAST/). Multiple sequence alignments of STY1365 amino acid sequences and EcolTa2 holin of E. coli TA271 (ZP_07522128.1), ESCE_1669 holin of E. coli SE11 (YP_002292944.1), ECDG_01257 holin of E. coli B185 (ZP_06657343.1) and holin 1 of phage ΦP27 (NP_543080.1) were constructed using vector nt suite v.8 software (Invitrogen). For the chromosomal deletion of STY1365, the ‘one step inactivation’ method described by Datsenko & Wanner (2000) was used. Following mutagenesis, the aph resistance cassette was removed by FLP-mediated recombination. The FRT site generated by excision of antibiotic resistance cassette was used to integrate plasmid pCE36, generating a transcriptional lacZY fusion (Ellermeier et al., 2002).

In summary, we found that human mucus influences the metabolism of B. longum biotype longum NCIMB8809 in a semi-defined medium. Concomitantly, an increase of glucose consumption was observed, together with a shift of glycosidase activities that could play a role in the degradation of the glycoprotein matrix of mucin. Furthermore, mucin-associated leucine was incorporated into the B. longum proteins www.selleckchem.com/MEK.html during growth, and some proteins that are likely to mediate interaction with mucus, as well as some others involved in the response to environmental challenges, were found to be differentially produced. The results shown here will contribute to understanding the interactions between human

mucus and intestinal Bifidobacterium. This work was financed by FEDER funds (European

Union) and the Spanish Plan Nacional de I+D+i through the project AGL2007-61805. L.R. was the recipient of a predoctoral I3P contract from CSIC, and M.G. was funded by a CSIC Intramural Project 2008-70049. “
“Using a previously developed in vitro model to characterize the enterocyte-adherent microbiota fraction, we explored the potential of the probiotic strain Bifidobacterium animalis ssp. lactis BI07 to modulate the inflammation-dependent dysbioses of the enterocyte-adherent microbiota from 12 healthy human donors. According to our findings, B. animalis ssp. lactis BI07 is effective in limiting the increase of pro-inflammatory pathobionts on the inflamed mucosal site, supporting the recovery of a mutualistic community. “
“Chromera http://www.selleckchem.com/products/Y-27632.html velia is evolutionarily the closest free-living and photosynthetic organism to the medically important

obligatory parasitic apicomplexans that cause diseases including malaria and toxoplasmosis. In this study, a novel oligonucleotide probe targeting C. velia’s small subunit ribosomal RNA was designed. To enable usage of this probe as a detection tool, a fluorescence in situ hybridization (FISH) IMP dehydrogenase protocol was optimized. The results obtained showed that when used in combination, the C. velia CV1 probe and optimized FISH protocol enabled efficient detection of C. velia in culture. This new technique will allow a better understanding of the ecological role of C. velia within the coral microhabitat. Recently, a unicellular alga, Chromera velia, was discovered in a homogenized hard coral (Moore et al., 2008). Since then, much emphasis has been placed on C. velia’s relationship to the medically important phylum of apicomplexan obligate parasites rather than on the lifestyle aspects of this intriguing alga itself (Okamoto & McFadden, 2008; Janouskovec et al., 2010; Woehle et al., 2011). As a result, the true ecological significance of C. velia within the coral is currently unclear. However, C. velia undergoes a diurnal transformation between a motile and immotile form, similar to that seen in a widespread coral symbiont, Symbiodinium sp. (Bourne et al., 2009; Guo et al., 2010; Obornik et al., 2011).