010) mg/L (P = 0.006). The mean cord:maternal ratio was 1.2 (90% CI 1.0–1.5). The viral load was <400 HIV-1 RNA copies/mL in 24 of 26 women in the third trimester, in 24 of 26 at delivery, and in 15 of 19 postpartum. Within-subject comparisons demonstrated significantly higher CL/F and significantly lower C24 during pregnancy; however, the C24

was well above the inhibitory concentration 50%, or drug concentration that suppresses viral replication by half (IC50) in all subjects. While we found higher emtricitabine CL/F and this website lower C24 and AUC during pregnancy compared with postpartum, these changes were not sufficiently large to warrant dose adjustment during pregnancy. Umbilical cord blood concentrations were similar to maternal concentrations. HIV-1-infected pregnant women commonly receive antiretroviral drugs. Combination antiretroviral regimens including nucleoside reverse transcriptase inhibitors (NRTIs) and either a protease inhibitor or a nonnucleoside reverse transcriptase inhibitor are recommended for pregnant women requiring antiretroviral therapy for their own health. In addition, women who do not meet criteria for treatment for their own health generally receive antiretrovirals for prevention of mother-to-child transmission of HIV-1 (HIV) [1]. Physiological changes during pregnancy affect antiretroviral drug disposition and

previous studies of antiretroviral pharmacology during pregnancy have shown reduced Liothyronine Sodium antenatal exposure for many antiretrovirals [2]. Cobimetinib Inadequate antiretroviral exposure during pregnancy may yield inadequate virological

control, increasing the risk of developing drug resistance mutations and of transmitting HIV to the infant. Understanding placental transfer of antiretrovirals to the foetus is of critical importance, as such transfer may subject the foetus to both the benefit of protection against HIV infection and the risk of potential antiretroviral toxicity [3, 4]. Before any antiretroviral can be used safely and effectively in pregnancy, its pharmacology must be studied in pregnant women [5]. Emtricitabine, an oral, synthetic, cytidine analogue NRTI with potent activity against HIV-1, is frequently used in pregnancy. In nonpregnant adults, emtricitabine is well absorbed and has low protein binding, and the labelled dose of 200 mg once daily results in an average area under the concentration versus time curve (AUC) of 10.0 ± 3.1 mg h/L [6]. This average is based on data from both women and men. In these studies, the pharmacokinetics of emtricitabine were similar in adult female and male patients, and the data were not presented separately for women and men. Emtricitabine is primarily eliminated unchanged in the urine, and its clearance is proportional to renal function.

010) mg/L (P = 0.006). The mean cord:maternal ratio was 1.2 (90% CI 1.0–1.5). The viral load was <400 HIV-1 RNA copies/mL in 24 of 26 women in the third trimester, in 24 of 26 at delivery, and in 15 of 19 postpartum. Within-subject comparisons demonstrated significantly higher CL/F and significantly lower C24 during pregnancy; however, the C24

was well above the inhibitory concentration 50%, or drug concentration that suppresses viral replication by half (IC50) in all subjects. While we found higher emtricitabine CL/F and selleck chemicals lower C24 and AUC during pregnancy compared with postpartum, these changes were not sufficiently large to warrant dose adjustment during pregnancy. Umbilical cord blood concentrations were similar to maternal concentrations. HIV-1-infected pregnant women commonly receive antiretroviral drugs. Combination antiretroviral regimens including nucleoside reverse transcriptase inhibitors (NRTIs) and either a protease inhibitor or a nonnucleoside reverse transcriptase inhibitor are recommended for pregnant women requiring antiretroviral therapy for their own health. In addition, women who do not meet criteria for treatment for their own health generally receive antiretrovirals for prevention of mother-to-child transmission of HIV-1 (HIV) [1]. Physiological changes during pregnancy affect antiretroviral drug disposition and

previous studies of antiretroviral pharmacology during pregnancy have shown reduced Anidulafungin (LY303366) antenatal exposure for many antiretrovirals [2]. Torin 1 Inadequate antiretroviral exposure during pregnancy may yield inadequate virological

control, increasing the risk of developing drug resistance mutations and of transmitting HIV to the infant. Understanding placental transfer of antiretrovirals to the foetus is of critical importance, as such transfer may subject the foetus to both the benefit of protection against HIV infection and the risk of potential antiretroviral toxicity [3, 4]. Before any antiretroviral can be used safely and effectively in pregnancy, its pharmacology must be studied in pregnant women [5]. Emtricitabine, an oral, synthetic, cytidine analogue NRTI with potent activity against HIV-1, is frequently used in pregnancy. In nonpregnant adults, emtricitabine is well absorbed and has low protein binding, and the labelled dose of 200 mg once daily results in an average area under the concentration versus time curve (AUC) of 10.0 ± 3.1 mg h/L [6]. This average is based on data from both women and men. In these studies, the pharmacokinetics of emtricitabine were similar in adult female and male patients, and the data were not presented separately for women and men. Emtricitabine is primarily eliminated unchanged in the urine, and its clearance is proportional to renal function.

010) mg/L (P = 0.006). The mean cord:maternal ratio was 1.2 (90% CI 1.0–1.5). The viral load was <400 HIV-1 RNA copies/mL in 24 of 26 women in the third trimester, in 24 of 26 at delivery, and in 15 of 19 postpartum. Within-subject comparisons demonstrated significantly higher CL/F and significantly lower C24 during pregnancy; however, the C24

was well above the inhibitory concentration 50%, or drug concentration that suppresses viral replication by half (IC50) in all subjects. While we found higher emtricitabine CL/F and ABT-263 research buy lower C24 and AUC during pregnancy compared with postpartum, these changes were not sufficiently large to warrant dose adjustment during pregnancy. Umbilical cord blood concentrations were similar to maternal concentrations. HIV-1-infected pregnant women commonly receive antiretroviral drugs. Combination antiretroviral regimens including nucleoside reverse transcriptase inhibitors (NRTIs) and either a protease inhibitor or a nonnucleoside reverse transcriptase inhibitor are recommended for pregnant women requiring antiretroviral therapy for their own health. In addition, women who do not meet criteria for treatment for their own health generally receive antiretrovirals for prevention of mother-to-child transmission of HIV-1 (HIV) [1]. Physiological changes during pregnancy affect antiretroviral drug disposition and

previous studies of antiretroviral pharmacology during pregnancy have shown reduced Protein kinase N1 antenatal exposure for many antiretrovirals [2]. CSF-1R inhibitor Inadequate antiretroviral exposure during pregnancy may yield inadequate virological

control, increasing the risk of developing drug resistance mutations and of transmitting HIV to the infant. Understanding placental transfer of antiretrovirals to the foetus is of critical importance, as such transfer may subject the foetus to both the benefit of protection against HIV infection and the risk of potential antiretroviral toxicity [3, 4]. Before any antiretroviral can be used safely and effectively in pregnancy, its pharmacology must be studied in pregnant women [5]. Emtricitabine, an oral, synthetic, cytidine analogue NRTI with potent activity against HIV-1, is frequently used in pregnancy. In nonpregnant adults, emtricitabine is well absorbed and has low protein binding, and the labelled dose of 200 mg once daily results in an average area under the concentration versus time curve (AUC) of 10.0 ± 3.1 mg h/L [6]. This average is based on data from both women and men. In these studies, the pharmacokinetics of emtricitabine were similar in adult female and male patients, and the data were not presented separately for women and men. Emtricitabine is primarily eliminated unchanged in the urine, and its clearance is proportional to renal function.

Saline soils are pristine and unexplored habitats representing intriguing ecosystems expected to harbour

potential diazotrophs capable of adapting in extreme conditions, and these implicated organisms are largely obscure. Differential occurrence of diazotrophs was studied by the nifH gene-targeted clone library approach. Four nifH gene clone libraries were constructed from different soil niches, that is saline soils (low and high salinity; EC 3.8 and 7.1 ds m−1), and agricultural and rhizosphere soil. Additionally, the abundance of diazotrophic community members was assessed Epigenetic inhibitor using quantitative PCR. Results showed environment-dependent metabolic versatility and the presence of nitrogen-fixing bacteria affiliated with a range of taxa, encompassing members of the Alphaproteobacteria, Betaproteobacteria, Deltaproteobacteria, Gammaproteobacteria, Cyanobacteria and Firmicutes. The analyses unveiled the dominance of Alphaproteobacteria and Gammaproteobacteria (Pseudomonas,

Halorhodospira, Ectothiorhodospira, Bradyrhizobium, Agrobacterium, Amorphomonas) as nitrogen fixers in coastal–saline soil ecosystems, and Alphaproteobacteria and Betaproteobacteria (Bradyrhizobium, Azohydromonas, Azospirillum, Ideonella) in agricultural/rhizosphere ecosystems. The results revealed a repertoire of novel nitrogen-fixing selleck bacterial guilds particularly in saline soil ecosystems. “
“Chair of Food Safety, Faculty of Veterinary Medicine, LMU, Oberschleißheim, Germany Ground feeds for pigs were investigated for fungal contamination before

and after pelleting (subsamples in total n = 24) by cultural and molecular biological methods. A fungal-specific primer pair ITS1/ITS5.8R was used to amplify fungal DNA; PCR products were processed for the PCR-SSCP method. In the resulting acrylamide gel, more than 85% of DNA bands of ground feeds were preserved after pelleting. Twenty-two DNA bands were sequenced; all represented fungal DNA. The level of fungal DNA in ground feed samples was equivalent to 4.77–5.69 log10 CFU g−1, calculated by qPCR using a standard curve of Aspergillus flavus. In pelleted IMP dehydrogenase feed, the level of fungal DNA was in average ± 0.07 log10 different from ground feed. Quantified by cultural methods, the fresh ground feeds contained up to 4.51 log10 CFU g−1 culturable fungi, while there was < 2.83 log10 CFU g−1 detected in pelleted feeds. This result shows that, while the process of pelleting reduced the amount of living fungi dramatically, it did not affect the total fungal DNA in feed. Thus, the described methodology was able to reconstruct the fungal microbiota in feeds and reflected a considerable fungal contamination of raw materials such as grains. "
“Glyphosate is a widely used herbicide that inhibits 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) activity. Most plants and microbes are sensitive to glyphosate.

Previous work has demonstrated that immediately following 21 days of self-administration, while blood levels of cocaine are still high, there are reductions in functional activity in a number of brain regions (Macey et al., 2004); however, the question remained as to whether these changes persisted beyond the self-administration session. Most functional activity studies determine the effects of a drug challenge; however, the present study focused on rates of local cerebral glucose utilization Obeticholic Acid order in the absence of drug, to determine

its residual effects. These data are important because determining the persistent effects of cocaine self-administration on functional activity can point to changes in specific brain regions and circuits which may be predictive of behavioral deficits in cocaine-addicted individuals. We show that cocaine self-administration results in functional reductions in brain regions involved in reward, learning and memory that are present 48 h after the final cocaine session. We also see reduced function of the dorsal raphe and locus coeruleus, which has implications for global brain function as

these nuclei have an extensive network of projections. this website Using behavioral activity analysis after cocaine self-administration we report alterations which could be predicted based on decreased serotonergic and dopaminergic functioning, demonstrating that these neural changes have behavioral implications. The Dipeptidyl peptidase reduced functional activity in selected regions suggests that even limited cocaine self-administration is capable of producing reductions in regional brain activity that

may have adverse consequences for normal functioning. Male, Sprague-Dawley rats (375–400 g; Harlan Laboratories, Frederick, MD, USA) were maintained according to the National Institutes of Health guidelines in Association for Assessment and Accreditation of Laboratory Animal Care-accredited facilities. The experimental protocol was approved by the Institutional Animal Care and Use Committee at Wake Forest School of Medicine. Rats (n = 14) were anesthetized with ketamine (100 mg/kg) and xylazine (10 mg/kg), implanted with chronic indwelling jugular catheters, and trained for i.v. self-administration as previously described (Liu et al., 2005). Following surgery, animals were singly housed, and all self-administration sessions took place in the home cage. Each animal was maintained on a reverse light cycle (03:00 h lights off; 15:00 h lights on), and all self-administration procedures occurred during the active/dark cycle. Sessions were 6 h in length and were terminated at the end of the 6 h or after 40 injections of drug. Animals self-administered cocaine (1.5 mg/kg per injection over 4 s) on a fixed-ratio 1 schedule of administration. Concurrent with the start of each injection, the lever retracted and a stimulus light was activated for 20 s to signal a time-out period.

aeruginosa, because functional analysis of VP1701, which is homologous to ExsC, is lacking and there is no ExsE homologue in the T3SS1 region. BIBW2992 concentration Here, we demonstrate that vp1701 and vp1702 are functional orthologues of exsC and exsE, respectively, of P. aeruginosa. VP1701 was required for the production of T3SS1-related proteins. VP1702 was a negative regulator for T3SS1-related protein production and was secreted

by T3SS1. We also found that H-NS represses T3SS1-related gene expression by suppressing exsA gene expression. These findings indicate that the transcription of V. parahaemolyticus T3SS1 genes is regulated by a dual regulatory system consisting of the ExsACDE regulatory cascade and H-NS. Vibrio parahaemolyticus, one of the human pathogenic vibrios, causes seafood-associated gastroenteritis (Honda & Iida, 1993). Although this microorganism is better known for causing gastroenteritis, it may also cause wound infection and septicemia (Ryan, 1976; Mertens et al., 1979; Daniels et al., 2000). It has been reported that clinical isolates of this organism have two sets of genes for separate type III secretion systems (T3SSs) on chromosomes 1 and 2 (T3SS1 and T3SS2, respectively) (Makino et al., 2003). A functional analysis of T3SS1 revealed that it predominantly contributes to V. parahaemolyticus-induced cytotoxicity in vitro and is involved Smad inhibitor in lethal activity in a murine infection model in vivo (Ono et al.,

2006; Hiyoshi et al., 2010). These results implicate T3SS1 in V. parahaemolyticus-induced septicemia in humans. The T3SS1 gene cluster of V. parahaemolyticus is composed of 42 genes, of which 30 genes are similar to those of the T3SS gene apparatus of Yersinia sp. and Pseudomonas aeruginosa (Makino et al., 2003; Park et al., 2004; Ono et al., 2006). In the middle

region of the T3SS1 gene cluster, there are 12 coding sequences (CDSs), which may encode effector proteins and their chaperones (Ono et al., 2006; Casselli et al., Selleck MG 132 2008; Akeda et al., 2009). At the terminus region of the T3SS1 gene cluster, there are three genes, VP1698, VP1699 and VP1701, that share sequence similarities with P. aeruginosa T3SS regulatory proteins ExsD (22% identity, 40% similarity), ExsA (45% identity, 64% similarity) and ExsC (32% identity, 48% similarity), respectively (Fig. 1a). The expression of P. aeruginosa T3SS is highly regulated and is induced by contact with host cells and low Ca2+ concentrations (Iglewski et al., 1978; Frank, 1997; Vallis et al., 1999). Transcription of the genes in the P. aeruginosa T3SS gene cluster is controlled by a regulatory cascade involving three interacting proteins (ExsC, ExsD and ExsE) that regulate ExsA transcriptional activity (Yahr & Wolfgang, 2006). ExsA is a member of the AraC family of transcriptional activators, and is a positive transcription activator required for the expression of all T3SS genes (Frank et al.

WB assays were reported as negative (without bands), positive [with at least two of the following bands: p24, glycoprotein 41 (gp41) and gp120/160] or indeterminate (with bands not meeting the criteria for positivity). The HIV prevalence was 10.4% (161 of 1549 patients) and the HIV incidence was 6.3% persons/year [6]. A total of 14 (0.9%) MSM had an HIV-indeterminate WB and, among the 1374 MSM with HIV-negative results, 16 (1.2%) had discordant results in the screening assay (12 were reactive by Ag-Ab ELISA, three were reactive by the particle agglutination assay, and one was reactive by both techniques,

but all were negative by WB) (Table 1). Three samples were not available for any of the tests and one was only available learn more for viral load measurement, so 14 HIV-negative WB samples with a discordant screening test and 13 HIV-indeterminate WB samples were examined for HIV nucleic acid detection using viral load testing [VERSANT® HIV-1 RNA 3.0 Assay Cytoskeletal Signaling inhibitor (bDNA); Siemens, Munich, Germany] and for p24 antigen using the ELISA technique (Vironostika HIV-1 Antigen; Biomerieux, Marcy l’Etoile, France). A group of

241 HIV-negative samples (with two negative screening assays) were also tested. Samples with viral load values < 200 HIV-1 RNA copies/mL were considered HIV-negative for the purpose of this study. Table 1 shows the results for each sample. One of 14 (7.1%) of the HIV-negative WB samples with discordant results in the screening assays had detectable nucleic acid/p24 antigen, and 23.1% (three of 13) of the HIV-indeterminate WB samples were also reactive for p24 antigen and had a viral load > 500 000 copies/mL. Overall, 14.8% (four of 27) of the samples with discordant or indeterminate results were identified as HIV-positive using direct diagnosis. Four new cases were identified by p24 antigen Dichloromethane dehalogenase and nucleic acid detection, increasing the HIV prevalence in these MSM by 0.3%, from 10.4% [95% confidence interval (CI) 8.8–11.9%] to 10.7% (95% CI 9.1–12.2%). Among the 241 HIV-negative samples, no

cases of viral load > 200 copies/mL were detected. Twenty-five patients had a detectable viral load with values < 200 copies/mL. Of these, 12 returned for further testing and were found to be negative for HIV infection. Out of a total of 16 patients with HIV-negative WB with discordant results in the screening assays, three (19%) returned for a further HIV test, and were found to be HIV-negative. Patient WB-neg 5, who was retrospectively found to be HIV-positive, did not return for a new diagnosis. Patient WB-neg 14, who had a viral load of 106 copies/mL, did not return. Of the 14 patients with indeterminate results, 12 (86%) returned to have their HIV status determined. Three of them were HIV-positive (WB-ind 1, WB-ind 4 and WB-ind 8) and nine were HIV-negative, including patients WB-ind 10 and WB-ind 13, who had viral load values of 135 and < 50 copies/mL, respectively.

Compared with the HIV-uninfected men in our sample, HIV-infected men were younger, with lower body mass index (BMI) and more often Black. HIV-infected men had lower FT (age-adjusted FT 88.7 ng/dL vs. 101.7 ng/dL in HIV-uninfected men; P = 0.0004); however, FT was not associated with CAC,

log carotid IMT, or the presence of carotid lesions. HIV status was not associated with CAC presence or log carotid IMT, but was associated with carotid lesion presence (adjusted odds ratio 1.69; 95% confidence interval 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men. Compared with HIV-uninfected men, HIV-infected men had lower FT, as well as more prevalent carotid lesions. In both groups, FT was not associated with CAC presence, log carotid IMT, or carotid

lesion presence, suggesting that FT does not influence subclinical CVD in selleck screening library this population of men with and at risk Stem Cells inhibitor for HIV infection. Increased rates of myocardial infarction and accelerated cardiovascular disease (CVD) progression have been observed among HIV-infected individuals [1], particularly among those taking antiretroviral therapy [2, 3]. Identifying modifiable CVD risk factors among individuals with HIV infection is important to decrease CVD risk. Several population-based studies have shown that low serum testosterone (T) is associated with increased all-cause mortality [4] and CVD-related

death [5] in men. Low serum T may be a risk factor for CVD by several mechanisms, including increased visceral adiposity (leading to glucose intolerance and diabetes mellitus), inflammation, and a more direct effect on the vasculature [6-8]. There is an increased prevalence of hypogonadism in HIV-infected men [9] and hypogonadism may persist despite effective antiretroviral therapy [10]. Although CVD in HIV-infected men may be a consequence of underlying viral mechanisms or antiretroviral therapy, it is crucial to investigate other clinically reversible factors such as low T that might result in an increased susceptibility to atherosclerotic disease. To our click here knowledge, this is the first investigation of the potential role of T in the pathogenesis of CVD in HIV-infected individuals. The aim of our study was to examine the relationship between free testosterone (FT) and early stages of CVD and to explore nontraditional risk factors for CVD in an HIV-infected population, using an HIV-uninfected comparison group. We used data from a subpopulation of the Multicenter AIDS Cohort Study (MACS; see Appendix) to assess the relationship between FT and coronary artery calcium (CAC) presence, carotid intima-media thickness (IMT), and carotid lesion presence among men with and at risk from HIV infection.

For example, and as we documented earlier (Hafed et al., 2011), our two monkeys showed different patterns

of microsaccades in the early cue-induced analysis intervals of Figs 8 and 9. The fact that the monkeys behaved similarly later in the trials (Fig. 10) might hint at some possible reasons for the earlier differences. One such reason could be related to the task design, in which the monkeys knew with 100% certainty that no perceptual discrimination stimuli could appear before ~1500 ms after cue onset. Thus, it may be the case that each monkey adopted a different strategy of ‘covertly’ inspecting the stimulus array at the Tofacitinib beginning of a trial, and that the patterns of microsaccades that we observed in this epoch revealed this difference. As a particular strategy was not reinforced this early in the trials, individual differences between the two monkeys in

the initial stages of the trial are conceivable. In contrast, at the ends of the trials (Fig. 10), when paying attention to the relevant locations was behaviorally reinforced in both monkeys, both of them showed RAD001 cell line similar patterns of microsaccade directions, and this was true for both the normal behavior without SC inactivation (Fig. 10A) (Hafed et al., 2011) and during SC inactivation (Fig. 10B). More importantly, the fact that SC inactivation resulted in a repulsion of microsaccades away from the affected region in both monkeys, despite their individual differences, supports the view that it is activity modulations in the peripheral SC that may be sufficient to bias the overall representation in the SC map and alter the triggering of microsaccades. This result may be interesting in the light of recent behavioral observations of a clear dissociation between microsaccade rate and microsaccade directions during covert visual attention tasks (Pastukhov & Braun, 2010; Pastukhov et al., 2012). It would be interesting to further test such a dissociation in the light of our results, especially because we also saw clear differences between the effects of peripheral SC inactivation on microsaccade rate and those on microsaccade direction. Finally, our results indicate that the multifaceted role

of the SC Histone demethylase in vision, cognition and oculomotor control contributes to the correlations between attentional cueing and microsaccades. In addition, these results can help to explain the reproducible, almost machine-like, manner in which stimulus transients, such as attentional cues, induce microsaccades (Hafed et al., 2011): this arises because of the sensitivity of the SC to such transients as well as its proximity to the motor output. However, these results also raise the question of why such a relationship exists in the first place. Given that microsaccades cause transient extra-retinal changes in vision (Zuber & Stark, 1966; Beeler, 1967; Hafed & Krauzlis, 2010) and concomitant changes in visual responses in the brain, including at the level of the SC (Martinez-Conde et al.

For example, and as we documented earlier (Hafed et al., 2011), our two monkeys showed different patterns

of microsaccades in the early cue-induced analysis intervals of Figs 8 and 9. The fact that the monkeys behaved similarly later in the trials (Fig. 10) might hint at some possible reasons for the earlier differences. One such reason could be related to the task design, in which the monkeys knew with 100% certainty that no perceptual discrimination stimuli could appear before ~1500 ms after cue onset. Thus, it may be the case that each monkey adopted a different strategy of ‘covertly’ inspecting the stimulus array at the FK506 in vitro beginning of a trial, and that the patterns of microsaccades that we observed in this epoch revealed this difference. As a particular strategy was not reinforced this early in the trials, individual differences between the two monkeys in

the initial stages of the trial are conceivable. In contrast, at the ends of the trials (Fig. 10), when paying attention to the relevant locations was behaviorally reinforced in both monkeys, both of them showed UK-371804 similar patterns of microsaccade directions, and this was true for both the normal behavior without SC inactivation (Fig. 10A) (Hafed et al., 2011) and during SC inactivation (Fig. 10B). More importantly, the fact that SC inactivation resulted in a repulsion of microsaccades away from the affected region in both monkeys, despite their individual differences, supports the view that it is activity modulations in the peripheral SC that may be sufficient to bias the overall representation in the SC map and alter the triggering of microsaccades. This result may be interesting in the light of recent behavioral observations of a clear dissociation between microsaccade rate and microsaccade directions during covert visual attention tasks (Pastukhov & Braun, 2010; Pastukhov et al., 2012). It would be interesting to further test such a dissociation in the light of our results, especially because we also saw clear differences between the effects of peripheral SC inactivation on microsaccade rate and those on microsaccade direction. Finally, our results indicate that the multifaceted role

of the SC DOK2 in vision, cognition and oculomotor control contributes to the correlations between attentional cueing and microsaccades. In addition, these results can help to explain the reproducible, almost machine-like, manner in which stimulus transients, such as attentional cues, induce microsaccades (Hafed et al., 2011): this arises because of the sensitivity of the SC to such transients as well as its proximity to the motor output. However, these results also raise the question of why such a relationship exists in the first place. Given that microsaccades cause transient extra-retinal changes in vision (Zuber & Stark, 1966; Beeler, 1967; Hafed & Krauzlis, 2010) and concomitant changes in visual responses in the brain, including at the level of the SC (Martinez-Conde et al.