Dr Malcolm von Schantz
Reader in Molecular Neurobiology
Qualifications: BSc MSc PhD FLS
Phone: Work: 01483 68 6468
Room no: 08 AY 02
- Reader in Molecular Neurobiology, University of Surrey, since 2009
- Senior Lecturer in Physiology and Biochemistry, University of Surrey
- Lecturer in Physiology and Biochemistry, University of Surrey
- Postdoctoral Fellow, Imperial College
- PhD, Gothenburg University
- MSc, Lund University
- BSc, Lund University
- Circadian rhythms
- Clock genes
- Molecular evolution
Current research funding
- United States Air Force Office of Scientific Research
- Royal Society
- Daiwa Foundation
- 'Mistimed sleep disrupts circadian regulation of the human transcriptome.'.
Proc Natl Acad Sci U S A, Full text is available at: http://epubs.surrey.ac.uk/805147/
Circadian organization of the mammalian transcriptome is achieved by rhythmic recruitment of key modifiers of chromatin structure and transcriptional and translational processes. These rhythmic processes, together with posttranslational modification, constitute circadian oscillators in the brain and peripheral tissues, which drive rhythms in physiology and behavior, including the sleep-wake cycle. In humans, sleep is normally timed to occur during the biological night, when body temperature is low and melatonin is synthesized. Desynchrony of sleep-wake timing and other circadian rhythms, such as occurs in shift work and jet lag, is associated with disruption of rhythmicity in physiology and endocrinology. However, to what extent mistimed sleep affects the molecular regulators of circadian rhythmicity remains to be established. Here, we show that mistimed sleep leads to a reduction of rhythmic transcripts in the human blood transcriptome from 6.4% at baseline to 1.0% during forced desynchrony of sleep and centrally driven circadian rhythms. Transcripts affected are key regulators of gene expression, including those associated with chromatin modification (methylases and acetylases), transcription (RNA polymerase II), translation (ribosomal proteins, initiation, and elongation factors), temperature-regulated transcription (cold inducible RNA-binding proteins), and core clock genes including CLOCK and ARNTL (BMAL1). We also estimated the separate contribution of sleep and circadian rhythmicity and found that the sleep-wake cycle coordinates the timing of transcription and translation in particular. The data show that mistimed sleep affects molecular processes at the core of circadian rhythm generation and imply that appropriate timing of sleep contributes significantly to the overall temporal organization of the human transcriptome.
- 'The effect of different photoperiods in circadian rhythms of Per3 knockout mice'.
BioMed Research International, 2014doi: 10.1155/2014/170795
The aim of this study was to analyse the circadian behavioural responses of mice carrying a functional knockout of the Per3 gene (P e r 3 - / -) to different light: dark (L: D) cycles. Male adult wild-type (WT) and P e r 3 - / - mice were kept under 12-hour light: 12-hour dark conditions (12L: 12D) and then transferred to either a short or long photoperiod and subsequently released into total darkness. All mice were exposed to both conditions, and behavioural activity data were acquired through running wheel activity and analysed for circadian characteristics during these conditions. We observed that, during the transition from 12L: 12D to 16L: 8D, P e r 3 - / - mice take approximately one additional day to synchronise to the new L: D cycle compared to WT mice. Under these long photoperiod conditions, P e r 3 - / - mice were more active in the light phase. Our results suggest that P e r 3 - / - mice are less sensitive to light. The data presented here provides further evidence that Per3 is involved in the suppression of behavioural activity in direct response to light. © 2014 D. S. Pereira et al.
- 'Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcriptome.'.
Proc Natl Acad Sci U S A, United States: 110 (12), pp. E1132-E1141.
Insufficient sleep and circadian rhythm disruption are associated with negative health outcomes, including obesity, cardiovascular disease, and cognitive impairment, but the mechanisms involved remain largely unexplored. Twenty-six participants were exposed to 1 wk of insufficient sleep (sleep-restriction condition 5.70 h, SEM = 0.03 sleep per 24 h) and 1 wk of sufficient sleep (control condition 8.50 h sleep, SEM = 0.11). Immediately following each condition, 10 whole-blood RNA samples were collected from each participant, while controlling for the effects of light, activity, and food, during a period of total sleep deprivation. Transcriptome analysis revealed that 711 genes were up- or down-regulated by insufficient sleep. Insufficient sleep also reduced the number of genes with a circadian expression profile from 1,855 to 1,481, reduced the circadian amplitude of these genes, and led to an increase in the number of genes that responded to subsequent total sleep deprivation from 122 to 856. Genes affected by insufficient sleep were associated with circadian rhythms (PER1, PER2, PER3, CRY2, CLOCK, NR1D1, NR1D2, RORA, DEC1, CSNK1E), sleep homeostasis (IL6, STAT3, KCNV2, CAMK2D), oxidative stress (PRDX2, PRDX5), and metabolism (SLC2A3, SLC2A5, GHRL, ABCA1). Biological processes affected included chromatin modification, gene-expression regulation, macromolecular metabolism, and inflammatory, immune and stress responses. Thus, insufficient sleep affects the human blood transcriptome, disrupts its circadian regulation, and intensifies the effects of acute total sleep deprivation. The identified biological processes may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness of sleep homeostasis, circadian rhythmicity, and metabolism.
- 'Circadian period and the timing of melatonin onset in men and women: predictors of sleep during the weekend and in the laboratory.'.
J Sleep Res, doi: 10.1111/jsr.12001
Sleep complaints and irregular sleep patterns, such as curtailed sleep during workdays and longer and later sleep during weekends, are common. It is often implied that differences in circadian period and in entrained phase contribute to these patterns, but few data are available. We assessed parameters of the circadian rhythm of melatonin at baseline and in a forced desynchrony protocol in 35 participants (18 women) with no sleep disorders. Circadian period varied between 23 h 50 min and 24 h 31 min, and correlated positively (n = 31, r(s) = 0.43, P = 0.017) with the timing of the melatonin rhythm relative to habitual bedtime. The phase of the melatonin rhythm correlated with the Insomnia Severity Index (n = 35, r(s) = 0.47, P = 0.004). Self-reported time in bed during free days also correlated with the timing of the melatonin rhythm (n = 35, r(s) = 0.43, P = 0.01) as well as with the circadian period (n = 31, r(s) = 0.47, P = 0.007), such that individuals with a more delayed melatonin rhythm or a longer circadian period reported longer sleep during the weekend. The increase in time in bed during the free days correlated positively with circadian period (n = 31, r(s) = 0.54, P = 0.002). Polysomnographically assessed latency to persistent sleep (n = 34, r(s) = 0.48, P = 0.004) correlated with the timing of the melatonin rhythm when participants were sleeping at their habitual bedtimes in the laboratory. This correlation was significantly stronger in women than in men (Z = 2.38, P = 0.017). The findings show that individual differences in circadian period and phase of the melatonin rhythm associate with differences in sleep, and suggest that individuals with a long circadian period may be at risk of developing sleep problems.
- 'Sleep, diurnal preference, health, and psychological well-being: a prospective single-allelic-variation study.'.
Chronobiol Int, England: 29 (2), pp. 131-146.
Individual differences in sleep and diurnal preference associate with physical and mental health characteristics, but few genetic determinants of these differences have been identified. A variable number tandem repeat (VNTR) polymorphism in the PERIOD3 (PER3) gene (rs57875989) has been reported to associate with diurnal preference, i.e., preferred timing of waking and sleep. Here, the authors investigate in a prospective single-candidate genetic variant study whether allelic variation for this polymorphism associates also with reported actual sleep timing and sleep duration, as well as psychological and health measures. Six hundred and seventy-five subjects, aged 20 to 35 yrs, completed questionnaires to assess sleep and psychological and health characteristics and were genotyped for the PER3 VNTR. Homozygosity for the longer allele (PER3(5/5)) of the VNTR was associated with increased morning preference, earlier wake time and bedtime, and reduced daytime sleepiness. Separate analyses of work and rest days demonstrated that the increase in time in bed during rest days was greatest in PER3(5/5) homozygotes. PER3 genotype modified the effects of sleep timing and duration on fluid intelligence and body mass index. Genotype was not associated with physical or psychological characteristics as assessed by the SF-36 Health Questionnaire, the General Health Questionnaire, the Big Five Inventory, the Behavioral Inhibition System-Behavioral Activation System scales, and the Positive and Negative Affect Scale, even though these measures varied significantly with diurnal preference as assessed by the Morningness-Eveningness Questionnaire. Whereas diurnal preference also predicts mental health and psychological characteristics, as well as sleep timing, the PER3 VNTR specifically affects measures of sleep timing and may also modify the effects of sleep on health outcome measures.
- 'Assessment of circadian rhythms in humans: comparison of real-time fibroblast reporter imaging with plasma melatonin.'.
FASEB J, doi: 10.1096/fj.11-201699
We compared the period of the rhythm of plasma melatonin, driven by the hypothalamic circadian pacemaker, to in vitro periodicity in cultured peripheral fibroblasts to assess the effects on these rhythms of a polymorphism of PER3 (rs57875989), which is associated with sleep timing. In vitro circadian period was determined using luminometry of cultured fibroblasts, in which the expression of firefly luciferase was driven by the promoter of the circadian gene Arntl (Bmal1). The period of the melatonin rhythm was assessed in a 9-d forced desynchrony protocol, minimizing confounding effects of sleep-wake and light-dark cycles on circadian rhythmicity. In vitro periods (32 participants, 24.61±0.33 h, mean±sd) were longer than in vivo periods (31 participants, 24.16±0.17 h; P<0.0001) but did not differ between PER3 genotypes (P>0.4). Analyses of replicate in vitro assessments demonstrated that circadian period was reproducible within individuals (intraclass correlation=0.62), but in vivo and in vitro period assessments did not correlate (P>0.9). In accordance with circadian entrainment theory, in vivo period correlated with the timing of melatonin (P<0.05) at baseline and with diurnal preference (P<0.05). Individual circadian rhythms can be reliably assessed in fibroblasts but may not correlate with physiological rhythms driven by the central circadian pacemaker.-Hasan, S., Santhi, N., Lazar, A.S., Slak, A., Lo, J., von Schantz, M., Archer, S. N., Johnston, J. D., Dijk, D.-J. Assessment of circadian rhythms in humans: comparison of real-time fibroblast reporter imaging with plasma melatonin.
- 'Effects of partial and acute total sleep deprivation on performance across cognitive domains, individuals and circadian phase.'.
PLoS One, United States: 7 (9)Full text is available at: http://epubs.surrey.ac.uk/802565/
Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate.
- 'Polymorphism in the PER3 Promoter Associates with Diurnal Preference and Delayed Sleep Phase Disorder'.
SLEEP, 33 (5), pp. 695-701.Full text is available at: http://epubs.surrey.ac.uk/207034/
Study Objectives: To screen the PER3 promoter for polymorphisms and investigate the phenotypic associations of these polymorphisms with diurnal preference, delayed sleep phase disorder/syndrome (DSPD/DSPS), and their effects on reporter gene expression. Design: Interspecific comparison was used to define the approximate extent of the PER3 promoter as the region between the transcriptional start site and nucleotide position −874. This region was screened in DNA pools using PCR and direct sequencing, which was also used to screen DNA from individual participants. The different promoter alleles were cloned into a luciferase expression vector and a deletion library created. Promoter activation was measured by chemiluminescence. Setting: N/A Patients or Participants: DNA samples were obtained from volunteers with defined diurnal preference (3 x 80, selected from a pool of 1,590), and DSPD patients (n = 23). Interventions: N/A Measurements and Results: We verified three single nucleotide polymorphisms (G −320T, C −319A, G −294A), and found a novel variable number tandem repeat (VNTR) polymorphism (−318 1/2 VNTR). The −320T and −319A alleles occurred more frequently in DSPD compared to morning (P = 0.042 for each) or evening types (P = 0.006 and 0.033). The allele combination TA2G was more prevalent in DSPD compared to morning (P = 0.033) or evening types (P = 0.002). Luciferase expression driven by the TA2G combination was greater than for the more common GC2A (P < 0.05) and the rarer TA1G (P < 0.001) combinations. Deletion reporter constructs identified two enhancer regions (−703 to −605, and −283 to −80). Conclusions: Polymorphisms in the PER3 promoter could affect its expression, leading to potential differences in the observed functions of PER3.
- 'Association between Specific Diurnal Preference Questionnaire Items and PER3 VNTR Genotype'.
CHRONOBIOLOGY INTERNATIONAL, 26 (3) Article number PII 910356950 , pp. 464-473.Full text is available at: http://epubs.surrey.ac.uk/804107/
- 'Phenotypic effects of genetic variability in human clock genes on circadian and sleep parameters'. JOURNAL OF GENETICS, 87 (5), pp. 513-519. . (2008)
- 'Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism'. SLEEP, 31 (8), pp. 1159-1167. . (2008)
- 'Inter-individual differences in habitual sleep timing and entrained phase of endogenous circadian rhythms of BMAL1, PER2 and PER3 mRNA in human leukocytes'.
SLEEP, 31 (5), pp. 608-617.Full text is available at: http://epubs.surrey.ac.uk/285505/
Study Objectives: Individual sleep timing differs and is governed partly by circadian oscillators, which may be assessed by hormonal markers, or by clock gene expression. Clock gene expression oscillates in peripheral tissues, including leukocytes. The study objective was to determine whether the endogenous phase of these rhythms, assessed in the absence of the sleep-wake and light-dark cycle, correlates with habitual sleep-wake timing. Design: Observational, cross-sectional. Setting: Home environment and Clinical Research Center. Participants: 24 healthy subjects aged 25.0 ± 3.5 (SD) years. Measurements: Actigraphy and sleep diaries were used to characterize sleep timing. Circadian rhythm phase and amplitude of plasma melatonin, cortisol, and BMAL1, PER2, and PER3 expression were assessed during a constant routine. Results: Circadian oscillations were more robust for PER3 than for BMAL1 or PER2. Average peak timings were 6:05 for PER3, 8:06 for PER2, 15:06 for BMAL1, 4:20 for melatonin, and 10:49 for cortisol. Individual sleep-wake timing correlated with the phases of melatonin and cortisol. Individual PER3 rhythms correlated significantly with sleep-wake timing and the timing of melatonin and cortisol, but those of PER2 and BMAL1 did not reach significance. The correlation between sleep timing and PER3 expression was stronger in individuals homozygous for the variant of the PER3 polymorphism that is associated with morningness. Conclusions: Individual phase differences in PER3 expression during a constant routine correlate with sleep timing during entrainment. PER3 expression in leukocytes represents a useful molecular marker of the circadian processes governing sleep-wake timing.
- 'PER3 polymorphism predicts sleep structure and waking performance'. CURRENT BIOLOGY, 17 (7), pp. 613-618. . (2007)
- 'Age-related change in the association between a polymorphism in the PER3 gene and preferred timing of sleep and waking activities'. JOURNAL OF SLEEP RESEARCH, 16 (1), pp. 12-16. . (2007)
- 'Conscientiousness is a predictor of diurnal preference.'.
Chronobiol Int, United States: 24 (6), pp. 1249-1254.Full text is available at: http://epubs.surrey.ac.uk/804106/
The relationship between diurnal preference, as measured by the Horne-Ostberg questionnaire, and quantifiable personality traits was investigated in 617 participants. A hierarchical multiple regression analysis demonstrated that out of the personality variables, conscientiousness was the single biggest predictor of diurnal preference (beta=0.246), after controlling for depression, sleep disorders, shift work, age, gender, and demographic characteristics. Morningness has previously been associated with physiological parameters of the circadian clock and with polymorphisms in circadian clock genes, suggesting the possibility that conscientiousness, too, may be linked to the same parameters.
- 'Evolutionary history of the vertebrate Period genes'. JOURNAL OF MOLECULAR EVOLUTION, 62 (6), pp. 701-707. . (2006)
- 'A silent polymorphism in the PER1 gene associates with extreme diurnal preference in humans'.
JOURNAL OF HUMAN GENETICS, 51 (12), pp. 1122-1125.Full text is available at: http://epubs.surrey.ac.uk/145882/
- 'Evolutionary history of the vertebrate Period genes'.
Journal of Molecular Evolution, 62 (6), pp. 701-707.
Circadian clock genes are remarkably conserved between eucoelomates. Although Drosophila has one copy of each major component, vertebrates have two or (in the case of the Period genes) three paralogs (Per1-3). We investigated the possibility that the vertebrate Per genes arose through two genome duplications during the emergence of vertebrates. Phylogenetic trees have placed zebrafish and mammalian Per1 and 2 together in a separate branch from Per3. The positions of four coding region splice sites were conserved between Drosophila per and the human paralogs, the fifth one being unique to Drosophila. The human PER genes shared the positions of all coding region splice sites, except the first two in PER1 and PER2 (which PER3 lacks). The phases of all splice sites were conserved between all four genes with two exceptions. Analysis of all genes within 10 Mb of the human PER1-3 genes, which are located 7.8-8.8 Mb from the telomeres on chromosomes 17, 2, and 1, identified several orthologous neighbors shared by at least two PER genes. Two gene families, HES (hairy and Enhancer of Split) and KIF1 (kinesin-like protein 1), were represented in all three of these paralogons. Although no functional fourth human PER paralog exists, five representatives from the same gene families were found close to the telomer of chromosome 3. We conclude that the ancestral chordate Per gene underwent two duplication events, giving rise to Per1-3 and a lost fourth paralog. © Springer Science+Business Media, Inc. 2006.
- 'Evolution of a length polymorphism in the human PER3 gene, a component of the circadian system'. JOURNAL OF BIOLOGICAL RHYTHMS, 20 (6), pp. 490-499. . (2005)
- 'Expansion during primate radiation of a variable number tandem repeat in the coding region of the circadian clock gene Period3'. JOURNAL OF BIOLOGICAL RHYTHMS, 20 (5), pp. 470-472. . (2005)
- 'A single-nucleotide polymorphism in the 5 '-untranslated region of the hPER2 gene is associated with diurnal preference'. JOURNAL OF SLEEP RESEARCH, 14 (3), pp. 293-297. . (2005)
- 'Timing and consolidation of human sleep, wakefulness, and performance by a symphony of oscillators'. JOURNAL OF BIOLOGICAL RHYTHMS, 20 (4), pp. 279-290. . (2005)
- 'Absence of phosphoglucose isomerase-1 in retinal photoreceptor, pigment epithelium and Muller cells'. EUROPEAN JOURNAL OF NEUROSCIENCE, 19 (11), pp. 2923-2930. . (2004)
- 'Clocks, genes and sleep'. JOURNAL OF THE ROYAL SOCIETY OF MEDICINE, 96 (10), pp. 486-489. . (2003)
- 'A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference'.
SLEEP, 26 (4), pp. 413-415.Full text is available at: http://epubs.surrey.ac.uk/2847/
- 'The 3111 Clock gene polymorphism is not associated with sleep and circadian rhythmicity in phenotypically characterized human subjects'. JOURNAL OF SLEEP RESEARCH, 11 (4), pp. 305-312. . (2002)
- 'Recent developments in circadian photoreception: More than meets the eye'. INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 41 (7), pp. 1605-1607. . (2000)
- 'Analysis of differentially expressed genes in the wildtype and rd mouse retina by macroarray screening.'. INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 41 (4), pp. S27-S27. . (2000)
- 'The putative brain photoperiodic photoreceptors in the vetch aphid, Megoura viciae'. JOURNAL OF INSECT PHYSIOLOGY, 45 (11), pp. 1011-1019. . (1999)
- 'Circadian oscillation of photopigment transcript levels in the mouse retina'. MOLECULAR BRAIN RESEARCH, 72 (1), pp. 108-114. . (1999)
- 'Regulation of mammalian circadian behavior by non-rod, non-cone, ocular photoreceptors'. SCIENCE, 284 (5413), pp. 502-504. . (1999)
- 'Extraocular light exposure does not suppress plasma melatonin in humans'.
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 83 (9), pp. 3369-3372.doi: 10.1210/jc.83.9.3369Full text is available at: http://epubs.surrey.ac.uk/207053/
- 'Cloning of a cyclic GMP phosphodiesterase gamma subunit from the ground squirrel retina'. MOLECULAR BRAIN RESEARCH, 54 (2), pp. 327-333. . (1998)
- 'Effects of circadian phase and prior partial sleep deprivation on executive functions during total sleep deprivation are modulated by PER3 polymorphism'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 41-41. . (2012)
- ''Trait-like' susceptibility to sleep loss varies with circadian phase and the task used to index vulnerable-resilient sleep-deprived performance'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 36-37. . (2012)
- 'The circadian and homeostatic regulation of sleep spindle activity: effect of the PER3 VNTR polymorphism'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 82-82. . (2012)
- 'PER3 polymorphism predictssusceptibility to sleep deprivation-induced impairment of early morning executive performance'. AMER ACADEMY SLEEP MEDICINE SLEEP, Minneapolis, MN: 21st Annual Meeting of the Association-Professional-Sleep-Societies 30, pp. A54-A54. . (2007)
- 'Endogenous circadian rhythm of PER3 RNA in human leucocytes: Association with sleep timing, melatonin rhythm, and PER3 genotype'. AMER ACADEMY SLEEP MEDICINE SLEEP, Minneapolis, MN: 21st Annual Meeting of the Association-Professional-Sleep-Societies 30, pp. A54-A55. . (2007)
- 'Genetic aspects of delayed sleep phase syndrome (DSPS)'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 5-5. . (2006)
- 'Polymorphism in the clock gene PER3 predicts sleep structure and EEG power spectra'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 53-53. . (2006)
- 'Age-related change in the association between a variable number tandem repeat polymorphism in the (PER3) gene and preferred timing of sleep and waking activities'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 97-98. . (2006)
- 'A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference'. AMER ACADEMY SLEEP MEDICINE SLEEP, CHICAGO, ILLINOIS: 17th Annual Meeting of the Associated-Professional-Sleep-Societies 26, pp. A109-A109. . (2003)
- 'Neuroleukin/AMF is present around cones and in various spatially restricted cell types of the mouse retina'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 44, pp. U459-U459. . (2003)
- 'Identification of transcripts enriched in the inner retina by differential macroarray hybridization'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 43, pp. U321-U321. . (2002)
- 'Identification of a novel retinal kinase with promoter elements affected by circadian clock proteins'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 43, pp. U308-U308. . (2002)
- 'Extraocular light exposure does not suppress plasma melatonin in humans'. SPRINGER BIOLOGIC EFFECTS OF LIGHT 1998, BASEL, SWITZERLAND: 5th International Arnold Rikli Symposium on the Biologic Effects of Light, pp. 403-406. . (1999)
- Level 1:
- BMS1008 Physiology
- Level 2:
- BMS2003 Molecular Biology and Genetics (Module Coordinator)
- BMS2008 Pathology & Medicine
- BMS2018 Key Skills (Module Coordinator)
- BMS2025 Neuroscience (Module Coordinator)
- Level 3:
- BMS3008 Neuroendocrinology
- BMS3034 Biological Rhythms
- BMS3038 Human and Medical Genetics
- BMS3042 Neuroscience: From Molecules to Mind
- Programme Organiser, MSc Clinical Biochemistry (until September 2009)
- Senior PTY Tutor (Overseas placements)
- Associate Dean (International Relations, from September 2009)
- Bioscience Erasmus Coordinator (from September 2009)
- Bioscience Library Representative
- Member of Senate