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Article ; Online: Visualization of sympathetic neural innervation in human white adipose tissue.

Perdikari, Aliki / Cacciottolo, Tessa / Henning, Elana / Mendes de Oliveira, Edson / Keogh, Julia M / Farooqi, I Sadaf

2022 Volume 12, Issue 3, Page(s) 210345

Abstract: Obesity, defined as an excess of adipose tissue that adversely affects health, is a major cause of morbidity and mortality. However, to date, understanding the structure and function of human adipose tissue has been limited by the inability to visualize ... ...

Abstract	Obesity, defined as an excess of adipose tissue that adversely affects health, is a major cause of morbidity and mortality. However, to date, understanding the structure and function of human adipose tissue has been limited by the inability to visualize cellular components due to the innate structure of adipocytes, which are characterized by large lipid droplets. Combining the iDISCO and the CUBIC protocols for whole tissue staining and optical clearing, we developed a protocol to enable immunostaining and clearing of human subcutaneous white adipose tissue (WAT) obtained from individuals with severe obesity. We were able to perform immunolabelling of sympathetic nerve terminals in whole WAT and subsequent optical clearing by eliminating lipids to render the opaque tissue completely transparent. We then used light sheet confocal microscopy to visualize sympathetic innervation of human WAT from obese individuals in a three-dimensional manner. We demonstrate the visualization of sympathetic nerve terminals in human WAT. This protocol can be modified to visualize other structures such as blood vessels involved in the development, maintenance and function of human adipose tissue in health and disease.
MeSH term(s)	Adipocytes ; Adipose Tissue ; Adipose Tissue, White/innervation ; Humans ; Obesity ; Sympathetic Nervous System/physiology
Language	English
Publishing date	2022-03-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.210345
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Article ; Online: Chromosomal deletions on 16p11.2 encompassing SH2B1 are associated with accelerated metabolic disease.

Hanssen, Ruth / Auwerx, Chiara / Jõeloo, Maarja / Sadler, Marie C / Henning, Elana / Keogh, Julia / Bounds, Rebecca / Smith, Miriam / Firth, Helen V / Kutalik, Zoltán / Farooqi, I Sadaf / Reymond, Alexandre / Lawler, Katherine

Cell reports. Medicine

2023 Volume 4, Issue 8, Page(s) 101155

Abstract: New approaches are needed to treat people whose obesity and type 2 diabetes (T2D) are driven by specific mechanisms. We investigate a deletion on chromosome 16p11.2 (breakpoint 2-3 [BP2-3]) encompassing SH2B1, a mediator of leptin and insulin signaling. ... ...

Abstract	New approaches are needed to treat people whose obesity and type 2 diabetes (T2D) are driven by specific mechanisms. We investigate a deletion on chromosome 16p11.2 (breakpoint 2-3 [BP2-3]) encompassing SH2B1, a mediator of leptin and insulin signaling. Phenome-wide association scans in the UK (N = 502,399) and Estonian (N = 208,360) biobanks show that deletion carriers have increased body mass index (BMI; p = 1.3 × 10
MeSH term(s)	Humans ; Leptin ; Diabetes Mellitus, Type 2/genetics ; Obesity/genetics ; Metabolic Diseases ; Insulins ; Adaptor Proteins, Signal Transducing
Chemical Substances	Leptin ; Insulins ; SH2B1 protein, human ; Adaptor Proteins, Signal Transducing
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2023.101155
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Article ; Online: Obesity due to melanocortin 4 receptor (MC4R) deficiency is associated with delayed gastric emptying.

Seelig, Eleonora / Henning, Elana / Keogh, Julia M / Gillett, Daniel / Shin, Evelyn / Buscombe, John / van der Klaauw, Agatha A / Farooqi, I Sadaf

Clinical endocrinology

2021 Volume 96, Issue 2, Page(s) 270–275

Abstract: Objective: People who are severely obese due to melanocortin-4 receptor (MC4R) deficiency experience hyperphagia and impaired fullness after a meal (satiety). Meal-induced satiety is influenced by hormones, such as peptide-YY (PYY), which are released ... ...

Abstract	Objective: People who are severely obese due to melanocortin-4 receptor (MC4R) deficiency experience hyperphagia and impaired fullness after a meal (satiety). Meal-induced satiety is influenced by hormones, such as peptide-YY (PYY), which are released by enteroendocrine cells upon nutrient delivery to the small intestine. Design: We investigated whether gastric emptying and PYY levels are altered in MC4R deficiency. Methods: Gastric emptying was measured with a gastric scintigraphy protocol using technetium-99m ( Results: We found that gastric emptying time was significantly delayed and percentage meal retention increased in individuals with MC4R deficiency compared to obese controls. In addition, fasting and mean PYY secretion throughout the day were decreased in MC4R deficiency, whereas postprandial PYY secretion was unaltered. Conclusion: Delayed gastric emptying and reduced basal PYY secretion may contribute to impaired satiety in people with obesity due to MC4R deficiency.
MeSH term(s)	Gastroparesis ; Humans ; Obesity ; Peptide YY ; Postprandial Period ; Receptor, Melanocortin, Type 4
Chemical Substances	MC4R protein, human ; Receptor, Melanocortin, Type 4 ; Peptide YY (106388-42-5)
Language	English
Publishing date	2021-10-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121745-8
ISSN	1365-2265 ; 0300-0664
ISSN (online)	1365-2265
ISSN	0300-0664
DOI	10.1111/cen.14615
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Article ; Online: Neural correlates of fat preference in frontotemporal dementia: translating insights from the obesity literature.

Ahmed, Rebekah M / Tse, Nga Yan / Chen, Yu / Henning, Elana / Hodges, John R / Kiernan, Matthew C / Irish, Muireann / Farooqi, I Sadaf / Piguet, Olivier

Annals of clinical and translational neurology

2021 Volume 8, Issue 6, Page(s) 1318–1329

Abstract: Objective: Alterations in eating behaviour are one of the diagnostic features of behavioural variant frontotemporal dementia (bvFTD). It is hypothesised that underlying brain network disturbances and atrophy to key structures may affect macronutrient ... ...

Abstract	Objective: Alterations in eating behaviour are one of the diagnostic features of behavioural variant frontotemporal dementia (bvFTD). It is hypothesised that underlying brain network disturbances and atrophy to key structures may affect macronutrient preference in bvFTD. We aimed to establish whether a preference for dietary fat exists in bvFTD, its association with cognitive symptoms and the underlying neural mechanisms driving these changes. Methods: Using a test meal paradigm, adapted from the obesity literature, with variable fat content (low 20%, medium 40% and high 60%), preference for fat in 20 bvFTD was compared to 16 Alzheimer's disease (AD) and 13 control participants. MRI brain scans were analysed to determine the neural correlates of fat preference. Results: Behavioural variant FTD patients preferred the high-fat meal compared to both AD (U = 61.5; p = 0.001) and controls (U = 41.5; p = 0.001), with 85% of bvFTD participants consistently rating the high-fat content meal as their preferred option. This increased preference for the high-fat meal was associated with total behavioural change (Cambridge Behavioural Inventory: r Conclusions: Increased preference for fat content is associated with many of the canonical features of bvFTD. These findings offer new insights into markers of disease progression and pathogenesis, providing potential treatment targets.
MeSH term(s)	Aged ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Amygdala/diagnostic imaging ; Amygdala/pathology ; Atrophy/pathology ; Cerebral Cortex/diagnostic imaging ; Cerebral Cortex/pathology ; Dietary Fats ; Female ; Food Preferences/physiology ; Frontotemporal Dementia/pathology ; Frontotemporal Dementia/physiopathology ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Nerve Net/diagnostic imaging ; Nerve Net/pathology ; Obesity ; Patient Acuity ; Putamen/diagnostic imaging ; Putamen/pathology
Chemical Substances	Dietary Fats
Language	English
Publishing date	2021-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.51369
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Article ; Online: Obesity Due to Steroid Receptor Coactivator-1 Deficiency Is Associated With Endocrine and Metabolic Abnormalities.

Cacciottolo, Tessa M / Henning, Elana / Keogh, Julia M / Bel Lassen, Pierre / Lawler, Katherine / Bounds, Rebecca / Ahmed, Rachel / Perdikari, Aliki / Mendes de Oliveira, Edson / Smith, Miriam / Godfrey, Edmund M / Johnson, Elspeth / Hodson, Leanne / Clément, Karine / van der Klaauw, Agatha A / Farooqi, I Sadaf

The Journal of clinical endocrinology and metabolism

2022 Volume 107, Issue 6, Page(s) e2532–e2544

Abstract: Context: Genetic variants affecting the nuclear hormone receptor coactivator steroid receptor coactivator, SRC-1, have been identified in people with severe obesity and impair melanocortin signaling in cells and mice. As a result, obese patients with ... ...

Abstract	Context: Genetic variants affecting the nuclear hormone receptor coactivator steroid receptor coactivator, SRC-1, have been identified in people with severe obesity and impair melanocortin signaling in cells and mice. As a result, obese patients with SRC-1 deficiency are being treated with a melanocortin 4 receptor agonist in clinical trials. Objective: Here, our aim was to comprehensively describe and characterize the clinical phenotype of SRC-1 variant carriers to facilitate diagnosis and clinical management. Methods: In genetic studies of 2462 people with severe obesity, we identified 23 rare heterozygous variants in SRC-1. We studied 29 adults and 18 children who were SRC-1 variant carriers and performed measurements of metabolic and endocrine function, liver imaging, and adipose tissue biopsies. Findings in adult SRC-1 variant carriers were compared to 30 age- and body mass index (BMI)-matched controls. Results: The clinical spectrum of SRC-1 variant carriers included increased food intake in children, normal basal metabolic rate, multiple fractures with minimal trauma (40%), persistent diarrhea, partial thyroid hormone resistance, and menorrhagia. Compared to age-, sex-, and BMI-matched controls, adult SRC-1 variant carriers had more severe adipose tissue fibrosis (46.2% vs 7.1% respectively, P = .03) and a suggestion of increased liver fibrosis (5/13 cases vs 2/13 in controls, odds ratio = 3.4), although this was not statistically significant. Conclusion: SRC-1 variant carriers exhibit hyperphagia in childhood, severe obesity, and clinical features of partial hormone resistance. The presence of adipose tissue fibrosis and hepatic fibrosis in young patients suggests that close monitoring for the early development of obesity-associated metabolic complications is warranted.
MeSH term(s)	Female ; Fibrosis ; Humans ; Male ; Nuclear Receptor Coactivator 1/genetics ; Obesity, Morbid/complications ; Obesity, Morbid/genetics
Chemical Substances	NCOA1 protein, human (EC 2.3.1.48) ; Nuclear Receptor Coactivator 1 (EC 2.3.1.48)
Language	English
Publishing date	2022-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgac067
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Article ; Online: The Impact of Acute Nutritional Interventions on the Plasma Proteome.

The Journal of clinical endocrinology and metabolism

2023 Volume 108, Issue 8, Page(s) 2087–2098

Abstract: Context: Humans respond profoundly to changes in diet, while nutrition and environment have a great impact on population health. It is therefore important to deeply characterize the human nutritional responses.: Objective: Endocrine parameters and ... ...

Abstract	Context: Humans respond profoundly to changes in diet, while nutrition and environment have a great impact on population health. It is therefore important to deeply characterize the human nutritional responses. Objective: Endocrine parameters and the metabolome of human plasma are rapidly responding to acute nutritional interventions such as caloric restriction or a glucose challenge. It is less well understood whether the plasma proteome would be equally dynamic, and whether it could be a source of corresponding biomarkers. Methods: We used high-throughput mass spectrometry to determine changes in the plasma proteome of i) 10 healthy, young, male individuals in response to 2 days of acute caloric restriction followed by refeeding; ii) 200 individuals of the Ely epidemiological study before and after a glucose tolerance test at 4 time points (0, 30, 60, 120 minutes); and iii) 200 random individuals from the Generation Scotland study. We compared the proteomic changes detected with metabolome data and endocrine parameters. Results: Both caloric restriction and the glucose challenge substantially impacted the plasma proteome. Proteins responded across individuals or in an individual-specific manner. We identified nutrient-responsive plasma proteins that correlate with changes in the metabolome, as well as with endocrine parameters. In particular, our study highlights the role of apolipoprotein C1 (APOC1), a small, understudied apolipoprotein that was affected by caloric restriction and dominated the response to glucose consumption and differed in abundance between individuals with and without type 2 diabetes. Conclusion: Our study identifies APOC1 as a dominant nutritional responder in humans and highlights the interdependency of acute nutritional response proteins and the endocrine system.
MeSH term(s)	Humans ; Male ; Proteome ; Diabetes Mellitus, Type 2 ; Proteomics ; Glucose ; Caloric Restriction
Chemical Substances	Proteome ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad031
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Article ; Online: A rare human variant that disrupts GPR10 signalling causes weight gain in mice.

Talbot, Fleur / Feetham, Claire H / Mokrosiński, Jacek / Lawler, Katherine / Keogh, Julia M / Henning, Elana / Mendes de Oliveira, Edson / Ayinampudi, Vikram / Saeed, Sadia / Bonnefond, Amélie / Arslan, Mohammed / Yeo, Giles S H / Froguel, Philippe / Bechtold, David A / Adamson, Antony / Humphreys, Neil / Barroso, Inês / Luckman, Simon M / Farooqi, I Sadaf

Nature communications

2023 Volume 14, Issue 1, Page(s) 1450

Abstract: Disruption of brain-expressed G protein-coupled receptor-10 (GPR10) causes obesity in animals. Here, we identify multiple rare variants in GPR10 in people with severe obesity and in normal weight controls. These variants impair ligand binding and G ... ...

Abstract	Disruption of brain-expressed G protein-coupled receptor-10 (GPR10) causes obesity in animals. Here, we identify multiple rare variants in GPR10 in people with severe obesity and in normal weight controls. These variants impair ligand binding and G protein-dependent signalling in cells. Transgenic mice harbouring a loss of function GPR10 variant found in an individual with obesity, gain excessive weight due to decreased energy expenditure rather than increased food intake. This evidence supports a role for GPR10 in human energy homeostasis. Therapeutic targeting of GPR10 may represent an effective weight-loss strategy.
MeSH term(s)	Animals ; Humans ; Mice ; Energy Metabolism ; Mice, Transgenic ; Obesity/genetics ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction ; Weight Gain/genetics
Chemical Substances	Receptors, G-Protein-Coupled ; PRLHR protein, human
Language	English
Publishing date	2023-03-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36966-3
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Article ; Online: Neural deletion of Sh2b1 results in brain growth retardation and reactive aggression.

Jiang, Lin / Su, Haoran / Keogh, Julia M / Chen, Zheng / Henning, Elana / Wilkinson, Paul / Goodyer, Ian / Farooqi, I Sadaf / Rui, Liangyou

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2018 Volume 32, Issue 4, Page(s) 1830–1840

Abstract: Psychiatric disorders are associated with aberrant brain development and/or aggressive behavior and are influenced by genetic factors; however, genes that affect brain aggression circuits remain elusive. Here, we show that neuronal Src-homology-2 (SH2)B ... ...

Abstract	Psychiatric disorders are associated with aberrant brain development and/or aggressive behavior and are influenced by genetic factors; however, genes that affect brain aggression circuits remain elusive. Here, we show that neuronal Src-homology-2 (SH2)B adaptor protein-1 ( Sh2b1) is indispensable for both brain growth and protection against aggression. Global and brain-specific deletion of Sh2b1 decreased brain weight and increased aggressive behavior. Global and brain-specific Sh2b1 knockout (KO) mice exhibited fatal, intermale aggression. In a resident-intruder paradigm, latency to attack was markedly reduced, whereas the number and the duration of attacks was significantly increased in global and brain-specific Sh2b1 KO mice compared with wild-type littermates. Consistently, core aggression circuits were activated to a higher level in global and brain-specific Sh2b1 KO males, based on c-fos immunoreactivity in the amygdala and periaqueductal gray. Brain-specific restoration of Sh2b1 normalized brain size and reversed pathologic aggression and aberrant activation of core aggression circuits in Sh2b1 KO males. SH2B1 mutations in humans were linked to aberrant brain development and behavior. At the molecular level, Sh2b1 enhanced neurotrophin-stimulated neuronal differentiation and protected against oxidative stress-induced neuronal death. Our data suggest that neuronal Sh2b1 promotes brain development and the integrity of core aggression circuits, likely through enhancing neurotrophin signaling.-Jiang, L., Su, H., Keogh, J. M., Chen, Z., Henning, E., Wilkinson, P., Goodyer, I., Farooqi, I. S., Rui, L. Neural deletion of Sh2b1 results in brain growth retardation and reactive aggression.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adult ; Aggression ; Animals ; Brain/growth & development ; Brain/metabolism ; Brain/physiology ; Child ; Female ; Gene Deletion ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Mutation ; PC12 Cells ; Rats
Chemical Substances	Adaptor Proteins, Signal Transducing ; SH2B1 protein, human ; Sh2bpsm1 protein, mouse
Language	English
Publishing date	2018-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201700831R
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Leptin-Mediated Changes in the Human Metabolome.

Lawler, Katherine / Huang-Doran, Isabel / Sonoyama, Takuhiro / Collet, Tinh-Hai / Keogh, Julia M / Henning, Elana / O'Rahilly, Stephen / Bottolo, Leonardo / Farooqi, I Sadaf

The Journal of clinical endocrinology and metabolism

2020 Volume 105, Issue 8

Abstract: Context: While severe obesity due to congenital leptin deficiency is rare, studies in patients before and after treatment with leptin can provide unique insights into the role that leptin plays in metabolic and endocrine function.: Objective: The aim ...

Abstract	Context: While severe obesity due to congenital leptin deficiency is rare, studies in patients before and after treatment with leptin can provide unique insights into the role that leptin plays in metabolic and endocrine function. Objective: The aim of this study was to characterize changes in peripheral metabolism in people with congenital leptin deficiency undergoing leptin replacement therapy, and to investigate the extent to which these changes are explained by reduced caloric intake. Design: Ultrahigh performance liquid chromatography-tandem mass spectroscopy (UPLC-MS/MS) was used to measure 661 metabolites in 6 severely obese people with congenital leptin deficiency before, and within 1 month after, treatment with recombinant leptin. Data were analyzed using unsupervised and hypothesis-driven computational approaches and compared with data from a study of acute caloric restriction in healthy volunteers. Results: Leptin replacement was associated with class-wide increased levels of fatty acids and acylcarnitines and decreased phospholipids, consistent with enhanced lipolysis and fatty acid oxidation. Primary and secondary bile acids increased after leptin treatment. Comparable changes were observed after acute caloric restriction. Branched-chain amino acids and steroid metabolites decreased after leptin, but not after acute caloric restriction. Individuals with severe obesity due to leptin deficiency and other genetic obesity syndromes shared a metabolomic signature associated with increased BMI. Conclusion: Leptin replacement was associated with changes in lipolysis and substrate utilization that were consistent with negative energy balance. However, leptin's effects on branched-chain amino acids and steroid metabolites were independent of reduced caloric intake and require further exploration.
MeSH term(s)	Adolescent ; Child ; Child, Preschool ; Chromatography, Liquid ; Energy Intake/drug effects ; Energy Metabolism/drug effects ; Female ; Hormone Replacement Therapy/methods ; Humans ; Leptin/administration & dosage ; Leptin/deficiency ; Leptin/genetics ; Lipolysis/drug effects ; Loss of Function Mutation ; Male ; Metabolome/drug effects ; Metabolomics ; Obesity/congenital ; Obesity/diagnosis ; Obesity/drug therapy ; Obesity/metabolism ; Recombinant Proteins/administration & dosage ; Severity of Illness Index ; Tandem Mass Spectrometry ; Treatment Outcome
Chemical Substances	LEP protein, human ; Leptin ; Recombinant Proteins
Language	English
Publishing date	2020-05-08
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgaa251
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Article ; Online: Oxytocin administration suppresses hypothalamic activation in response to visual food cues.

van der Klaauw, Agatha A / Ziauddeen, Hisham / Keogh, Julia M / Henning, Elana / Dachi, Sekesai / Fletcher, Paul C / Farooqi, I Sadaf

Scientific reports

2017 Volume 7, Issue 1, Page(s) 4266

Abstract: The aim of this study was to use functional neuroimaging to investigate whether oxytocin modulates the neural response to visual food cues in brain regions involved in the control of food intake. Twenty-four normal weight volunteers received intranasal ... ...

Abstract	The aim of this study was to use functional neuroimaging to investigate whether oxytocin modulates the neural response to visual food cues in brain regions involved in the control of food intake. Twenty-four normal weight volunteers received intranasal oxytocin (24 IU) or placebo in a double-blind, randomized crossover study. Measurements were made forty-five minutes after dosing. On two occasions, functional MRI (fMRI) scans were performed in the fasted state; the blood oxygen level-dependent (BOLD) response to images of high-calorie foods versus low-calorie foods was measured. Given its critical role in eating behaviour, the primary region of interest was the hypothalamus. Secondary analyses examined the parabrachial nuclei and other brain regions involved in food intake and food reward. Intranasal oxytocin administration suppressed hypothalamic activation to images of high-calorie compared to low-calorie food (P = 0.0125). There was also a trend towards suppression of activation in the parabrachial nucleus (P = 0.0683). No effects of intranasal oxytocin were seen in reward circuits or on ad libitum food intake. Further characterization of the effects of oxytocin on neural circuits in the hypothalamus is needed to establish the utility of targeting oxytocin signalling in obesity.
MeSH term(s)	Adult ; Brain Mapping ; Cues ; Feeding Behavior/drug effects ; Feeding Behavior/psychology ; Female ; Food ; Functional Neuroimaging ; Healthy Volunteers ; Humans ; Hypothalamus/drug effects ; Hypothalamus/physiology ; Male ; Middle Aged ; Oxytocin/administration & dosage ; Photic Stimulation ; Young Adult
Chemical Substances	Oxytocin (50-56-6)
Language	English
Publishing date	2017-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-04600-0
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