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Insulin-Like Growth Factors
Published in Jason Kelley, Cytokines of the Lung, 2022
Alan D. Stiles, Billie M. Moats-Staats, George Z. Retsch-Bogart
A more complex system to study combined endocrine and autocrine-paracrine production and action of IGFs is provided by a transgenic mouse line that overexpresses a human IGF-I gene (Mathews et al., 1988; Behringer et al., 1990). Because the IGF-I transgene is expressed with tissues that normally synthesize IGF-I, it may more closely resemble IGF-I physiology. The IGF-I serum concentrations are modestly higher (50%) than in littermates not carrying the transgene. Expression of the IGF-I transgene was present in all tissues examined, and IGF-I transgenic mice grow to be about 30% larger than littermates not carrying the transgene. Some asymmetry of somatic and organ growth was observed, consistent with the IGF-I infusion experiments in rats. For example, the increase in liver size was less than that of the body as a whole, whereas brain size was increased more than somatic size.
You Are What You Eat
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
All living organisms are composed of cells. The human brain has some 100 billion specialized cells called neurons. Big brains come at a significant cost because neurons are relative energy gluttons (Table 3.1). Comparing ourselves with nonhuman primates of similar body size (chimpanzees), brain size is twofold to threefold higher in humans. At birth, the human brain weighs about 500 grams, or 15% of typical newborn body mass, and that brain may account for up to 85% of the total energy budget or metabolic rate. By age 2, the brain has grown to near the adult size (modifications of brain connectivity continue at least into late adolescence), whereas the body is still only about 20% of adult size. This large and disproportionate early development of the brain in humans poses uniquely large demands on energy intake by human infants. This is manifest prenatally as rapid fetal development, assimilating nutrients circulating in the mother’s blood stream. Postnatally, these demands are met by innate behaviors and digestive systems that are optimal for obtaining and absorbing nutrients from milk, traditionally provided by the mother. In Chapter 8, we discuss the ontogeny of feeding in infants and children. Maternal milk is an animal source food (ASF) high in fat and energy density that provides all of the necessary nutrients for growth until the infant is able to be weaned to fully independent feeding.
Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
The Sacher hypothesis is intellectually exciting, at least to your author. Sacher terms it the “longevity-assurance hypothesis”, and does not deign to elevate it to the more lofty position of a “theory”. The underlying concepts are that every species evolved molecular and organizational stability to assure survival. There is, furthermore, no ontological reality to aging—each species evolves its own aging process. There is no accumulation of aging genes to be switched on or off. What does accumulate is the imperfect execution of functions. The rate and amount of DNA repair correlate with lifespan. In the evolutionary scheme, Sacher points out that humans live twice as long as apes and our DNA repair rate is twice as good. It is likely that the homonids branched off the pongid line about 15 to 20 million years ago, as based on the fossil record and the current similarities in man and ape DNA. Most of the hominid increase in brain size occurred in the last 2 million years, as well as most of man’s lifespan increase. Since this is very rapid indeed from the standpoint of evolution, it would indicate that a relatively small number of genes are involved in longevity. Sacher basically suggests that aging studies seek longevity assurance genes and not senescence genes.
Cortical and cerebellar structural correlates of cognitive-motor integration performance in females with and without persistent concussion symptoms
Published in Brain Injury, 2023
Johanna M. Hurtubise, Diana J. Gorbet, Loriann Hynes, Alison K. Macpherson, Lauren E. Sergio
The cerebellum (including brainstem) was extracted using the Spatially Unbiased Atlas Template (SUIT) toolbox within the Statistical Parametric Mapping software (SPM12; http://www.fil.ion.ucl.ac.uk/spm/, installed in MATLAB version 2014, Natick, Massachusetts, The MathWorks, Inc), and left in subject space (51). Total cerebellum volume (including total white matter and gray matter) was calculated using the Oxford Center for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Software Library (FSL, v5.0) (40). A ratio of cerebellum volume to brain size was then calculated as a proportion of the TIV (to account for differences in brain sizes between participants). The cerebellum was further parcellated into 28 lobules using SUIT-cerebellum within SPM12 (52). The volume of each lobule was then corrected for TIV using a proportion method.
Development of an adverse outcome pathway for radiation-induced microcephaly via expert consultation and machine learning
Published in International Journal of Radiation Biology, 2022
Thomas Jaylet, Roel Quintens, Mohamed Abderrafi Benotmane, Jukka Luukkonen, Ignacia Braga Tanaka, Chrystelle Ibanez, Christelle Durand, Magdalini Sachana, Omid Azimzadeh, Christelle Adam-Guillermin, Knut Erik Tollefsen, Olivier Laurent, Karine Audouze, Olivier Armant
As a well-known mutagen, IR induces microcephaly. Compelling evidence from human epidemiological studies and laboratory animals exposed in utero demonstrated the link between radiation-induced DNA damage and apoptosis of progenitors in the mouse cerebral cortex as the origin of microcephaly (Nowak et al. 2006; Saha et al. 2014; Barazzuol and Jeggo 2016; Kashiwagi et al. 2018; Mfossa et al. 2020). Microcephaly is observed after exposure throughout the neurogenesis period, from E11 to E17 in the mice and between weeks 8 and 25 of gestation in humans (Verreet et al. 2016), and is apparent in the domain of the low dose radiation (near 0.2 Gy for humans and 0.3 Gy for the mouse). In both species, the decreased brain size was strongly correlated to altered cognitive performance (Verreet et al. 2016; 2016). Importantly, the central role of TP53-induced apoptosis was demonstrated by transcriptome-wide expression studies of TP53 early transcriptional response to radiation exposure in mouse (Quintens et al. 2015; Mfossa et al. 2020) and zebrafish (Jaafar et al. 2013). Moreover, the partial rescue of the microcephaly phenotype when conditional Trp53 knock out mice are exposed to IR, provides a direct causal link between radiation-induced apoptosis and microcephaly (Mfossa et al. 2020).
Reference biometry of foetal brain by prenatal MRI and the distribution of measurements in foetuses with ventricular septal defect
Published in Annals of Medicine, 2021
Feng Xia, Yu Guo, Hua He, Peiwen Chen, Jianbo Shao, Wei Xia
Our data presented a prenatal MRI biometry of the foetal brain from a large cohort (n = 218) including FOD, BPD, and TCD from 18 to 37 gestational weeks. In order to represent our data from multiple perspectives, we showed mean, SD, maximum, minimum, 95% predicted confidence intervals (along with the regression equation) and the 3rd, 10th, 25th, 50th, 75th, 90th, 97th centiles of our measurements. The data of our study reflected the development of the brain itself, but not the skull. As we know, ultrasound biometry could only reflect the size of the skull, while MRI provides the possibility to display the actual size of the brain. It is important to know the brain size when we have to evaluate the development of the brain itself, for instance, in the condition of congenital heart diseases. The gestational age arranged from 18 to 37 weeks, as it’s recommended that prenatal MRI should be performed after 18 gestational weeks, not only for safety, but also for valuable additional information it could provide after 18 gestational weeks [25].