Protein concentrations were measured

using the Bradford method with bovine serum albumin as the standard (Bradford, 1976). Pi concentrations were determined using the molybdenum-blue method (Clesceri et al., 1989). Escherichia coli cells grown overnight on the 2 × YT medium with shaking at 37 °C were collected by centrifugation. The pellet was washed twice with Pi-free MOPS medium and resuspended in the same medium containing 2 mM glycerol-3-phosphate to an OD600 nm of 0.2. Samples taken from the cultures were centrifuged, and the supernatants Gefitinib were assayed for Pi. The Pfam database (Finn et al., 2008) indicated that E. coli YjbB consists of two distinct segments (Fig. 1). The N-terminal half of YjbB contains hydrophobic amino acid Dabrafenib datasheet residues whose sequence is conserved among eukaryotic type II Na+/Pi cotransporters and is designated the Na+/Pi cotransporter domain (Pfam accession number PF02690). Most Na+/Pi cotransporter proteins consist of two

repeats of this domain. In fact, the N-terminal half of YjbB also consists of two repeats of the Na+/Pi cotransporter domain (41% identity over 135 amino acids and 32% identity over 126 amino acids, respectively). The C-terminal half of YjbB contains two repeats of a PhoU domain (Pfam accession number PF01895) (21% identity over 80 amino acids and 15% identity over 60 amino acids, respectively), although the homology was considered insignificant in the database. Similarly, PhoU proteins also consist of two copies of the PhoU domain that form three-helix bundles (Liu et al., 2005; Oganesyan et al., 2005). This analysis suggested that YjbB might be involved both in Pi transport and in the regulation of Pho regulon genes. PhoU negatively regulates the Pho regulon genes (Wanner, 1996). We have reported that a phoU mutant, MT29, accumulated 1000-fold higher levels of polyP than the wild type due to the constitutive expression of pstSCAB (Morohoshi et al., 2002). To test whether the overproduction of YjbB can compensate for the loss of PhoU function, we introduced yjbB on a multicopy plasmid (pMWyjbB) into MT29. MT29 carrying pMWyjbB

had significantly lower levels of polyP (Table 2). One possible explanation for the reduction of polyP by YjbB is that the PhoU domain of YjbB Aurora Kinase had compensated for the chromosomal phoU mutation as a multicopy suppressor and reduced the expression of the Pho regulon genes. Because the phoA gene (alkaline phosphatase) is also one of the Pho regulon genes, we measured the alkaline phosphatase activity of MT29 carrying pMWyjbB. Unexpectedly, the levels of alkaline phosphatase activity were still high in the transformant, but they were reduced when pMWphoU was introduced (Table 2). It therefore seemed unlikely that YjbB overproduction reduced the expression of the Pho regulon genes. In other words, the reduced levels of polyP may not be due to the suppression of the increased expression of the PstSCAB Pi uptake system.

Heart rate was also positively correlated with total AMS symptom score; in contrast, fluid intake was Talazoparib in vitro negatively

correlated with total AMS symptom score. When investigating the symptom of high altitude headache alone (model 2 in Table 2), upper respiratory symptoms and stool consistency (where a higher number defines a looser stool) were correlated with headache severity, as did arterial oxygen saturation. However, when investigating presence or absence of clinically defined AMS (model 3 in Table 2), only upper respiratory symptoms (positive correlation) and arterial oxygen saturation (negative correlation) were significant predictors. Odds ratios suggested that a 1 unit increase in upper respiratory symptoms was associated with a 1.040 (1.005–1.262) significantly higher odds of having AMS; a 1 unit decrease in arterial oxygen saturation was associated with a 1.068 (1.000–1.141) significantly higher odds of having AMS. Time-lag models, which investigated whether variables predicted AMS the following day as required to infer causality, explained between 10 and 24% of variance in AMS (Table 3). The following day’s total AMS symptom score was positively correlated with upper respiratory symptoms (model 4 in Table 3). Heart rate and fluid intake also predicted future AMS symptoms. Thus, an increase of upper respiratory symptoms by 5 units

would increase total AMS symptom score the following day by 0.72 units (0.54–0.89); an increase in heart rate of 10 beats per min would

increase AMS score by 0.18 units (0.08–0.28); and a decrease of 10 mL per kg of body mass of fluid E7080 mw intake per day (∼710 mL per day) would increase total AMS score by 0.07 units (0.01–0.12). When investigating the symptom of high altitude headache alone, only arterial oxygen saturation was negatively correlated with the following day’s headache severity (model 5 in Table 3). Thus, a decrease in arterial oxygen saturation of 5% would increase headache severity most the next day by 0.06 units (0.02–0.10). This study is the first to use a longitudinal multiple regression analysis of daily illnesses and mental disturbances recorded during a relatively large expedition to high altitude. AMS affected almost half of the expedition participants, with up to one quarter having AMS on any day. However, AMS incidence alone underestimated the total illness symptom burden: all the participants also had upper respiratory symptoms, two thirds had loose stools and one third had diarrhea, and almost everyone reported mild anxiety. Upper respiratory symptoms increased as altitude was gained, and anxiety was also increased on certain days at high altitude. Detailed description of illnesses revealed that the variable contributing most to AMS symptom burden was difficulty sleeping. However, difficulty sleeping was also the least sensitive of the AMS symptoms to altitude change.

Secretion of the translational fusions corresponding to the four proteins was easily detected under these conditions (Fig. 1a). Another band, probably due to the degradation of the fused Mlr6331, was detected only in the pellet, indicating that the presence of the complete fused protein in the supernatant was not because of bacterial lysis. Fusions were also integrated into the chromosome of the rhcN mutant strain already containing pMP2112 (rhcN6316SRpMP2112, rhcN6331SRpMP2112, rhcN6358SRpMP2112, and rhcN6361SRpMP2112). No secretion was observed for any of them (Fig. 2b). These results

demonstrate that secretion of the translational fusions corresponding to mlr6361, mlr6358, mlr6316, and mlr6331, chromosomally integrated in the wild-type (wt) strain, occurs in a T3SS-dependent manner. Previous reports have indicated click here that mutations in protein secretion systems in M. loti affect symbiotic competitiveness in lotus (Hubber et al., 2004; Sánchez et al., 2009). Mesorhizobium loti MAFF303099 rhcN mutant was less competitive than the wt strain with regard to nodulation on Lo. tenuis cv. Pampa INTA (Sánchez et al., 2009). Because it has been reported that the M. loti T3SS mutant has different nodulation efficacies on different Lotus species (Okazaki et al., 2010), we decided to compare the symbiotic competitiveness of the wt with that of rhcN mutant strains on Lo. japonicus Miyacojima MG-20. As shown in

Fig. 2a, the strains showed no differences C-X-C chemokine receptor type 7 (CXCR-7) in competitiveness when they were co-inoculated NVP-BGJ398 datasheet in this plant. As the two strains differ in their protein secretion capacity, the lack of differences in competitiveness in the co-inoculation assays could be due to phenotypic complementation. We thus performed a nodulation test to compare the nodulation efficiency of the wt with that of rhcN mutant strains on Lo. japonicus MG-20 and found no significant differences between strains (Fig. 2b). Also, we analyzed the competitiveness of the wt and rhcN mutant strains on Lo. tenuis cv. Esmeralda, and in contrast to that observed on Lo. tenuis cv. Pampa INTA, the mutant was more competitive than the wt strain in this variety (Fig. 2a). This result indicates

that the inability to secrete some effectors, or to surface-expressed T3SS pili components, favors the M. loti’s competitive ability on Lo. tenuis cv. Esmeralda. To determine the role of the four M. loti T3SS putative effectors in the nodulation process, we performed nodulation competitive assays on Lo. tenuis cv. Esmeralda and Lo. japonicus MG-20 with the wt and single, double, and triple mutant strains. Co-inoculation experiments were carried out using different combinations of the strains analyzed. Surprisingly, the mutant deficient in three of the putative T3SS effectors (M. loti mlr6358/mlr6361/mlr6316, hereafter triple mutant) showed a significant decrease in competitiveness compared to the wt strain on both Lo. tenuis cv. Esmeralda (Fig. 3a) and Lo.

4). PSD analysis of the fragments revealed the partial structures reported in Table 2. From the sequences of these products, sakacin A also seems to elicit proteolytic activity, with a preference for the bond formed by the N-acetyl muramic acid (NAM)-linked FG-4592 l-alanine residue nearest to the polysaccharide chain in the peptoglycan. Thus, the specific action of sakacin A on Listeria cell walls resulted in breakdown of the peptoglycan component in a fashion similar to lysozyme, but with a different specificity. The purification of sakacin A produced by L. sakei DSMZ 6333 from bacteria cultured in a low-cost media formulation, based on industrial ingredients and/or residuals from agro-food production

(Trinetta et al., 2008a), through the procedure reported here, compares favorably with protocols

using higher-cost media and resulting in lower purification yields. The availability of significant amounts of purified sakacin A made it possible to investigate its mode of action. We confirmed sakacin A as a membrane-active bacteriocin that kills Listeria cells by making their membranes permeable (Kaiser & Montville, 1996; Ennahar et al., 1998). The cytoplasmic membrane seems the primary target of sakacin A, whose action is enhanced when cells are energized, possibly because transmembrane gradients favor the bacteriocin selleck chemical interaction with the membrane. The sakacin A action is straightforward and intense: both ΔΨ and ΔpH are completely dissipated in seconds, resulting in leakage of cellular material (McAuliffe et al., 1998). One suggested mechanism of action for class IIa bacteriocins is the ‘barrel-stave model’ that implies an electrostatic binding step mediated by a membrane-bound receptor followed by a step involving hydrophobic interaction of an amphiphilic bacteriocin domain with the lipid acyl chains and in pore formation (Ennahar et al., 1998; Drider et al., 2006). However, other hypothetical

mechanisms of action for class II bacteriocins imply a direct effect on cell walls (Kabuki et al., 1997; Nielsen et al., 2003). Our observations, obtained with a highly purified bacteriocin preparation, support that cell walls are a target for sakacin A. A similar mode of action was shown by enterolysin A on Listeria this website innocua cell walls, where the activity was muralytic (Nielsen et al., 2003). Enterococcus mundtii ST15 produced a bacteriocin active against Gram-positive and Gram-negative bacteria that displays a lytic action toward growing cells of Lactobacillus casei (De Kwaadsteniet et al., 2005). El Ghachi et al. (2006) investigated the lytic action of colicin M on Escherichia coli cell walls by HPLC and MALDI-TOF MS analysis, similar to our study. The data presented here confirm a slow hydrolytic action of sakacin A toward Listeria cell walls and suggest that sakacin A can break specific peptide bonds in the peptoglycan structure.

In order to assess in which FOR the BOLD activity associated with covert search in the anterior insula and the SEF was modulated, we calculated the percentage signal change for the ROIs in these two areas in both hemispheres (see Supporting

Information Fig. S1). These ROIs were defined by comparing covert search with the control condition (see ‘Materials and methods’). In all four ROIs, covert search seemed to evoke larger higher BOLD responses than the control condition (see Supporting Information Fig. S1). However, one-way anova across the different search conditions did not yield a significant modulation of the signal change (P > 0.1 for all find more four ROIs). Hence, the search related BOLD response in both the anterior insula and the SEF does not encode the FOR in which covert search operates. We tried to identify the FOR for covert serial search by studying the dependence of cortical BOLD activity, evoked by visual search, on eye-gaze position. Our key observation was that specific parts of the IPS and the right FEF showed a higher BOLD response during covert search to eye-centred contralateral locations, independent of

eye position. In other words, objects singled out in a search array by covert serial search are represented in an eye-centred or retinal coordinate system. However, compared with the left IPS, this effect was weaker in the right pIPS. Early and later Epacadostat cell line visual regions similarly exhibited stronger responses for covert

search directed to contralateral eye-centred locations, as expected from their known retinotopic organization. The anterior insula and the SEF did not show the above-mentioned eye-centred modulation of their search related response. Although not very likely, we admit that with the paradigm used we cannot exclude that a modification related to an effector such as the hand or the head could have had a modulatory effect on the clearly eye-centred BOLD responses, which we observed. However, in our paradigm the non-eye-centred search array location did not have any influence on the results, so we think that it is unlikely, though in principle possible to expect different results by changing the head or body position in our experiment. In the following discussion we will first address the question: can our findings based on BOLD responses be reconciled with single-unit studies Branched chain aminotransferase on covert visual search? We will then discuss how the evidence for eye-centred coding of covert search provided by our study fits with previous fMRI studies that addressed the reference frame for the encoding of covert as well as overt shifts of attention, i.e. saccades. This comparison seems pertinent, given the fact that overt and covert shifts of attention are tightly coupled and, moreover, usually assumed to share most of their cortical (Rizzolatti et al., 1987; Corbetta et al., 1998) and subcortical (Ignashchenkova et al., 2004) substrates.

In order to assess in which FOR the BOLD activity associated with covert search in the anterior insula and the SEF was modulated, we calculated the percentage signal change for the ROIs in these two areas in both hemispheres (see Supporting

Information Fig. S1). These ROIs were defined by comparing covert search with the control condition (see ‘Materials and methods’). In all four ROIs, covert search seemed to evoke larger higher BOLD responses than the control condition (see Supporting Information Fig. S1). However, one-way anova across the different search conditions did not yield a significant modulation of the signal change (P > 0.1 for all Selleck PD-332991 four ROIs). Hence, the search related BOLD response in both the anterior insula and the SEF does not encode the FOR in which covert search operates. We tried to identify the FOR for covert serial search by studying the dependence of cortical BOLD activity, evoked by visual search, on eye-gaze position. Our key observation was that specific parts of the IPS and the right FEF showed a higher BOLD response during covert search to eye-centred contralateral locations, independent of

eye position. In other words, objects singled out in a search array by covert serial search are represented in an eye-centred or retinal coordinate system. However, compared with the left IPS, this effect was weaker in the right pIPS. Early and later Selleckchem SP600125 visual regions similarly exhibited stronger responses for covert

search directed to contralateral eye-centred locations, as expected from their known retinotopic organization. The anterior insula and the SEF did not show the above-mentioned eye-centred modulation of their search related response. Although not very likely, we admit that with the paradigm used we cannot exclude that a modification related to an effector such as the hand or the head could have had a modulatory effect on the clearly eye-centred BOLD responses, which we observed. However, in our paradigm the non-eye-centred search array location did not have any influence on the results, so we think that it is unlikely, though in principle possible to expect different results by changing the head or body position in our experiment. In the following discussion we will first address the question: can our findings based on BOLD responses be reconciled with single-unit studies MycoClean Mycoplasma Removal Kit on covert visual search? We will then discuss how the evidence for eye-centred coding of covert search provided by our study fits with previous fMRI studies that addressed the reference frame for the encoding of covert as well as overt shifts of attention, i.e. saccades. This comparison seems pertinent, given the fact that overt and covert shifts of attention are tightly coupled and, moreover, usually assumed to share most of their cortical (Rizzolatti et al., 1987; Corbetta et al., 1998) and subcortical (Ignashchenkova et al., 2004) substrates.

5 h. HRP-conjugated donkey anti-goat was used as the secondary antibody and the reaction was developed with a TMB substrate (Tiangen). After 15 min of color development, the stop solution (8.5 M acetic acid, 2.5 M H2SO4) was added and the A450 nm

was recorded. The binding of HDL to the GAS (Type M6 and M41) was tested using GAS cells that were either immobilized onto microplate wells or were in suspension. GAS cell suspensions were added to microplate wells and incubated at room temperature for 1.5 h. Wells were washed and blocked overnight with 200 μL of 1% bovine serum albumin (BSA) in TBS or TBST at 4 °C. HDL binding was performed as described above in the rScl1 binding ELISA. selleck chemicals For the HDL binding to GAS cells in suspension, cells were incubated for 1.5 h with 1% BSA in TBS or TBST. After washing with TBS or TBST, 100 μL of human plasma was added to 1 mL of the cells. Following a 1-h incubation at room temperature, bacterial cells were pelleted and washed three times with TBS or TBST. After the final centrifugation, cell-bound proteins were dissociated Selleckchem PD-332991 from the cells by the incubation with 200 μL of 0.1 M glycine-HCl solution, pH 2, for 15 min. Bacterial cells were then removed by centrifugation and the proteins in the supernatant were precipitated with 10% TCA and analyzed by SDS-PAGE and immunoblotting. Electroblotting was carried out at a constant voltage

of 30 V for 1 h to transfer ApoAI and at a constant current of 300 mA for 3 h to transfer ApoB100. The immunodetection of ApoAI was performed with a goat anti-ApoAI antibody, followed by HRP-conjugated donkey Suplatast tosilate anti-goat secondary antibody as described above. The presence of ApoB100 was tested with a goat anti-LDL antibody (Chemicon, CA), followed by HRP-conjugated donkey anti-goat antibody (R&D Systems), and the detection was performed with chemiluminescence reagent (Tiangen). Results were expressed as mean±SD. Statistical significance was calculated

using two-tailed Student’s t-test for comparisons of two groups and Student–Neuman–Keuls for comparison of multiple groups, respectively. It was reported previously that several Scl1 proteins interact with LDL/ApoB100 via globular noncollagenous V regions (Han et al., 2006a). Here, we are testing the hypothesis that the Scl1.41 variant possess binding ability to HDL. Recombinant Scl1 (rScl1) proteins C176, C176V, and C176T were constructed, which are derived from Scl1.41 protein of GAS M41-type strain ATCC12373. PCR-amplified DNA fragments corresponding to a full-length or a partial scl1.41-gene sequence were cloned, expressed, and purified in E. coli BL21 (Table 1; Fig. 1a). rScl1 proteins were immobilized onto Strep-Tactin columns through their C-terminal tags (Strep-tag II) and these affinity columns were used to detect Scl1 ligands in human plasma. Human plasma (0.5 mL) was applied to these columns, including the control column without the rScl1 protein.

Tsror et al. (2001) reported that the application of Trichoderma harzianum in furrows reduced the incidence of black scurf significantly as compared with its application to the soil surface, which showed a relatively small effect. In summary, our results demonstrated that all fungi tested are effective for controlling R. solani diseases on potato. In our view, some constraints that could limit their effectiveness are rhizosphere

complexity and soil environment. In this context, their adaptability to field conditions, their toxicity for humans and animals as formulated products, and their time of application should be studied. This Z-VAD-FMK work was supported by the NSERC discovery grant to M.H. We thank the Canada Foundation for Innovation (CFI) for confocal microscopy facility support. We also thank Amandine Honore for technical assistance and Dr David Morse for comments and English editing. “
“This study was designed to evaluate gene expression patterns of the planktonic and biofilm cells of Staphylococcus aureus and SalmonellaTyphimurium in trypticase soy broth adjusted to pH 5.5 and pH 7.3. The planktonic Ixazomib datasheet and biofilm cells of multiple antibiotic-resistant S. aureus (S. aureusR) and S. Typhimurium (S. TyphimuriumR) were more resistant to β-lactams than those of antibiotic-susceptible

S. aureus (S. aureusS) and S. Typhimurium (S. TyphimuriumS) at pH 5.5 and pH 7.3. The relative gene expression levels of norB, norC, and mdeA genes were increased by 7.0-, 4.7-, and 4.6-fold, respectively,

in the biofilm cells of S. aureusS grown at pH 7.3, while norB, norC, mdeA, sec, seg, sei, sel, sem, sen, and seo genes were stable in the biofilm cells of S. aureusR. This study provides useful information for understanding gene expression patterns in the planktonic Reverse transcriptase and biofilm cells of antibiotic-resistance pathogens exposed to acidic stress. Over the last decades, the prevalence of antibiotic-resistant bacterial infections has been rapidly increased because of the repeated and prolonged use of antibiotics, leading to a serious health problem worldwide (Wegener, 2003; Gootz, 2010). The emergence of antibiotic-resistant bacteria has become of great concern for public health, which widely appears as frequent outbreaks in recent years (Boonmar et al., 1998; Van et al., 2007). Therefore, prevention strategies for antibiotic resistance are essential to control the spread of antibiotic-resistant pathogens. However, the discovery and development of novel antibiotics has lagged behind the emergence of antibiotic-resistant pathogens because of the lengthy and expensive processes, requiring phases of clinical investigation trials to obtain approval, and the lack of information on the antibiotic resistance mechanisms (Yineyama & Katsumata, 2006).

Tsror et al. (2001) reported that the application of Trichoderma harzianum in furrows reduced the incidence of black scurf significantly as compared with its application to the soil surface, which showed a relatively small effect. In summary, our results demonstrated that all fungi tested are effective for controlling R. solani diseases on potato. In our view, some constraints that could limit their effectiveness are rhizosphere

complexity and soil environment. In this context, their adaptability to field conditions, their toxicity for humans and animals as formulated products, and their time of application should be studied. This Dabrafenib clinical trial work was supported by the NSERC discovery grant to M.H. We thank the Canada Foundation for Innovation (CFI) for confocal microscopy facility support. We also thank Amandine Honore for technical assistance and Dr David Morse for comments and English editing. “
“This study was designed to evaluate gene expression patterns of the planktonic and biofilm cells of Staphylococcus aureus and SalmonellaTyphimurium in trypticase soy broth adjusted to pH 5.5 and pH 7.3. The planktonic see more and biofilm cells of multiple antibiotic-resistant S. aureus (S. aureusR) and S. Typhimurium (S. TyphimuriumR) were more resistant to β-lactams than those of antibiotic-susceptible

S. aureus (S. aureusS) and S. Typhimurium (S. TyphimuriumS) at pH 5.5 and pH 7.3. The relative gene expression levels of norB, norC, and mdeA genes were increased by 7.0-, 4.7-, and 4.6-fold, respectively,

in the biofilm cells of S. aureusS grown at pH 7.3, while norB, norC, mdeA, sec, seg, sei, sel, sem, sen, and seo genes were stable in the biofilm cells of S. aureusR. This study provides useful information for understanding gene expression patterns in the planktonic Oxalosuccinic acid and biofilm cells of antibiotic-resistance pathogens exposed to acidic stress. Over the last decades, the prevalence of antibiotic-resistant bacterial infections has been rapidly increased because of the repeated and prolonged use of antibiotics, leading to a serious health problem worldwide (Wegener, 2003; Gootz, 2010). The emergence of antibiotic-resistant bacteria has become of great concern for public health, which widely appears as frequent outbreaks in recent years (Boonmar et al., 1998; Van et al., 2007). Therefore, prevention strategies for antibiotic resistance are essential to control the spread of antibiotic-resistant pathogens. However, the discovery and development of novel antibiotics has lagged behind the emergence of antibiotic-resistant pathogens because of the lengthy and expensive processes, requiring phases of clinical investigation trials to obtain approval, and the lack of information on the antibiotic resistance mechanisms (Yineyama & Katsumata, 2006).

In subcortical brain parenchyma, Cx26-positive puncta were often co-localized with astrocytic Cx43, and some were localized along astrocyte cell bodies and processes immunolabelled for glial fibrillary acidic

protein. Cx26-positive puncta were also co-localized with punctate labelling of Cx47 around Ruxolitinib clinical trial oligodendrocyte somata. Comparisons of Cx26 labelling in rodent species revealed a lower density of Cx26-positive puncta and a more restricted distribution in subcortical regions of mouse compared with rat brain, perhaps partly explaining reported difficulties in detection of Cx26 in mouse brain parenchyma using antibodies or Cx26 gene reporters. These results support our earlier observations of Cx26 expression in astrocytes Talazoparib and its ultrastructural localization in individual

gap junction plaques formed between astrocytes as well as in heterotypic gap junctions between astrocytes and oligodendrocytes. “
“Ghrelin is an orexigenic hormone produced by the stomach. Ghrelin, however, may also be a modulator of the circadian system given that ghrelin receptors are expressed in the master clock, the suprachiasmatic nucleus (SCN) and several outputs of this region. To investigate this, we performed analyses of running wheel activity and neuronal activation in wild type (WT) and growth hormone secretagogue receptor-knockout (GHSR-KO) mice under various lighting conditions. GHSR-KO and WT mice were maintained under constant dark (DD) or constant light (LL) with ad libitum access to food before being placed

on a schedule of temporally restricted access to food (4 h/day) for 2 weeks. There were no differences between KO and WT mice in free-running period under DD, but GHSR-KO mice required more days to develop a high level of food anticipatory activity, and this was lower than that observed in WT mice. Under LL, GHSR-KO mice showed greater activity overall, lengthening of their circadian period, and more resistance to the disorganisational RAS p21 protein activator 1 effects of LL. Furthermore, GHSR-KO mice showed greater activity overall, and greater activity in anticipation of a scheduled meal under LL. These behavioral effects were not correlated with changes in the circadian expression of the Fos, Per1 or Per2 proteins under any lighting conditions. These results suggest that the ghrelin receptor plays a role in modulating the activity of the circadian system under normal conditions and under restricted feeding schedules, but does so through mechanisms that remain to be determined. The circadian system controls daily rhythms of rest and activity, hormones, and motivated behaviors like feeding. Light is the primary synchroniser of the master circadian clock, the suprachiasmatic nucleus (SCN) (Reppert & Weaver, 2002). However, feeding also synchronises circadian rhythms (Stephan, 2002).