Birth, Lucid Dream and the OBE

Honegger (1983) recently put forward the theory that the OBE is a form of lucid dream in which the cord, tunnel and out—of—body imagery result from a fetal OBE occurring during the stress of birth. This theory pre-dicts that people born by Caesarean section should be less likely to have these experiences

“With The Eyes of the Mind: An Empirical Analysis of Out-of-Body States" by Glen O. Gabbard and Stuart W. Twenlow

With the Eyes of the Mind is the first book on OBEs written by practicing psychiatrists; a fact which is both its strength and its weakness. It is full of interesting survey results as well as fascinating case material, but its theoretical contribution is narrowly psychoanalytic and displays little understanding of broader psychological and parapsychological perspectives

Mental Models in Sleep: Why Do We Feel More Conscious in Lucid Dreams?

Why do I seem to be more conscious in a lucid dream? I mean, that's what happens, isn't it? There you are dreaming away, ridiculous and quite unaware that it is a dream and suddenly you seem to be there. It's as though you've woken up in the middle of a dream, only of course the body hasn't. What has changed? I realize that I can't come to grips with what this question means. To ask, "why am I more conscious in a lucid dream?", begs a whole load of questions about consciousness, about "I", the nature of self, and about what it could possibly mean for something to be more or less conscious. It's a horrible question. Nevertheless, I will have a go at answering it

Plant Ultrastructure in the Scanning Electron Microscope

Preparative techniques which have been used to study internal details of plant cells in the scanning electron microscope are reviewed. A number of methods have previously been described which involve selective extraction of materials from freeze-fractured surfaces and can be referred to as freeze-fracture and cytoplasmic maceration. One of these techniques which involves an extended period of cytoplasmic maceration with dilute osmium tetroxide has been applied to the study of Cichorium intybus (chicory) pollen ontogeny. The results obtained, including changes in the numbers of mitochondria and the form of endoplasmic reticulum during the course of development demonstrate the value of the approach in showing the three dimensional arrangement of organelles and wall layers. The findings emphasise that pollen grains with similar mature morphologies may differ in the details of their ontogeny

Programming of cardiovascular disease across the life-course.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality, affecting both developed and developing countries. Whilst it is well recognized that our risk of CVD can be determined by the interaction between our genetics and lifestyle, this only partly explains the variability at the population level. Based on these well-known risk factors, for many years, intervention and primary prevention strategies have focused on modifying lifestyle factors in adulthood. However, research shows that our risk of CVD can be pre-determined by our early life environment and this area of research is known as the Developmental Origins of Health and Disease. The aim of this review is to evaluate our current understanding of mechanisms underlying the programming of CVD. This article is part of a special issue entitled CV Aging.H.L. Blackmore is funded by the British Heart Foundation. S.E. Ozanne is a member of the MRC Metabolic Diseases Unit and funded by MRC grantMC_UU_12012/4.This is the accepted manuscript of a paper published in the Journal of Molecular and Cellular Cardiology (Blackmore HL, Ozanne SE, Journal of Molecular and Cellular Cardiology 2014, doi:10.1016/j.yjmcc.2014.12.006)

Experiments in artificial culture: from noisy imitation to storytelling robots

This paper presents a series of experiments in collective social robotics, spanning more than 10 years, with the long-term aim of building embodied models of (aspects) of cultural evolution. Initial experiments demonstrated the emergence of behavioural traditions in a group of social robots programmed to imitate each other's behaviours (we call these Copybots). These experiments show that the noisy (i.e. less than perfect fidelity) imitation that comes for free with real physical robots gives rise naturally to variation in social learning. More recent experimental work extends the robots' cognitive capabilities with simulation-based internal models, equipping them with a simple artificial theory of mind. With this extended capability we explore, in our current work, social learning not via imitation but robot-robot storytelling, in an effort to model this very human mode of cultural transmission. In this paper we give an account of the methods and inspiration for these experiments,the experiments and their results, and an outline of possible directions for this programme of research. It is our hope that this paper stimulates not only discussion but suggestions for hypotheses to test with the Storybots

Maternal diet-induced obesity programs cardiovascular dysfunction in adult male mouse offspring independent of current body weight.

This is the final published version. It first appeared at http://press.endocrine.org/doi/abs/10.1210/en.2014-1383?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed.Obese pregnancies are not only associated with adverse consequences for the mother but also the long-term health of her child. Human studies have shown that individuals from obese mothers are at increased risk of premature death from cardiovascular disease (CVD), but are unable to define causality. This study aimed to determine causality using a mouse model of maternal diet-induced obesity. Obesity was induced in female C57BL/6 mice by feeding a diet rich in simple sugars and saturated fat 6 weeks prior to pregnancy and throughout pregnancy and lactation. Control females were fed laboratory chow. Male offspring from both groups were weaned onto chow and studied at 3, 5, 8, and 12 weeks of age for gross cardiac morphometry using stereology, cardiomyocyte cell area by histology, and cardiac fetal gene expression using qRT-PCR. Cardiac function was assessed by isolated Langendorff technology at 12 weeks of age and hearts were analyzed at the protein level for the expression of the β1 adrenergic receptor, muscarinic type-2 acetylcholine receptor, and proteins involved in cardiac contraction. Offspring from obese mothers develop pathologic cardiac hypertrophy associated with re-expression of cardiac fetal genes. By young adulthood these offspring developed severe systolic and diastolic dysfunction and cardiac sympathetic dominance. Importantly, cardiac dysfunction occurred in the absence of any change in corresponding body weight and despite the offspring eating a healthy low-fat diet. These findings provide a causal link to explain human observations relating maternal obesity with premature death from CVD in her offspring.HLB, YN and JLTA are funded by the British Heart Foundation. DFT is supported by the MRC Metabolic Diseases Unit. DAG is a Lister Institute Fellow and Royal Society Wolfson Merit Award Holder and is supported by the British Heart Foundation. SEO is a British Heart Foundation Senior Fellow and a member of the MRC Metabolic Diseases Unit

Maternal Metformin Intervention during Obese Glucose-Intolerant Pregnancy Affects Adiposity in Young Adult Mouse Offspring in a Sex-Specific Manner.

BackgroundMetformin is commonly used to treat gestational diabetes mellitus. This study investigated the effect of maternal metformin intervention during obese glucose-intolerant pregnancy on the gonadal white adipose tissue (WAT) of 8-week-old male and female mouse offspring.MethodsC57BL/6J female mice were provided with a control (Con) or obesogenic diet (Ob) to induce pre-conception obesity. Half the obese dams were treated orally with 300 mg/kg/d of metformin (Ob-Met) during pregnancy. Gonadal WAT depots from 8-week-old offspring were investigated for adipocyte size, macrophage infiltration and mRNA expression of pro-inflammatory genes using RT-PCR.ResultsGestational metformin attenuated the adiposity in obese dams and increased the gestation length without correcting the offspring in utero growth restriction and catch-up growth caused by maternal obesity. Despite similar body weight, the Ob and Ob-Met offspring of both sexes showed adipocyte hypertrophy in young adulthood. Male Ob-Met offspring had increased WAT depot weight (p p p F4/80 (p ConclusionsMaternal metformin intervention during obese pregnancy causes excessive adiposity, adipocyte hyperplasia and WAT inflammation in male offspring, highlighting sex-specific effects of prenatal metformin exposure on offspring WAT

Poor maternal nutrition programmes a pro-atherosclerotic phenotype in ApoE-/- mice.

Numerous animal studies have consistently shown that early life exposure to LP (low-protein) diet programmes risk factors for CVD (cardiovascular disease) such as dyslipidaemia, high BP (blood pressure) and cardiac dysfunction in the offspring. However, studies on the effect of maternal under-nutrition on offspring development of atherosclerosis are scarce. Applying our LP model to the ApoE(-/-) atherosclerosis-prone mouse model, we investigated the development of atherosclerotic lesions in the aortic root of 6-month-old offspring. In addition, markers of plaque progression including SMA (smooth muscle actin) and Mac3 (macrophage marker 3) were studied. Pregnant dams were fed on a control (20% protein) or on an isocaloric LP diet (8% protein) throughout pregnancy and lactation. After weaning, male offspring were maintained on 20% normal laboratory chow. At 6 months of age, LP offspring showed a significantly greater plaque area (P<0.05) with increased cholesterol clefts and significantly higher indices of DNA damage compared with controls (P<0.05). The expression of HMG-CoA reductase (3-hydroxy-3-methyl-glutaryl-CoA reductase) (P<0.05) and LDL (low-density lipoprotein) receptor in the liver of LP offspring were increased. Furthermore, LP offspring had higher LDL-cholesterol levels (P<0.05) and a trend towards elevated insulin. There were no differences in other lipid measurements and fasting glucose between groups. These observations suggest that early exposure to an LP diet accelerates the development and increases the progression of atherosclerotic lesions in young adult offspring. Future studies are needed to elucidate the specific mechanisms linking in utero exposure to a diet low in protein to the development of atherosclerosis.This work was supported by the British Heart Foundation [grant numbers FS/09/029/27902, FS/09/050], the Biotechnology and Biological Sciences Research Council and the Cambridge Commonwealth Trust