INTRA-UTERINE UNDERNUTRITION AND BRAIN DEVELOPMENT

PEDIATRICS ◽  
1971 ◽  
Vol 47 (3) ◽  
pp. 491-500
Author(s):  
H. Peter Chase ◽  
Carol S. Dabiere ◽  
N. Noreen Welch ◽  
Donough O'Brien
Keyword(s):  
Body Weight ◽  
Guinea Pig ◽  
Brain Development ◽  
Protein Content ◽  
In Utero ◽  
Brain Weight ◽  
Brain Growth ◽  
Maternal Malnutrition ◽  
Wet Weight ◽  
The Brain

The guinea pig, like the human, initiates the period of rapid brain growth in utero and thus provides a model for measuring the effects of maternal malnutrition on intra-uterine brain growth. In these studies the newborn of undernourished guinea pig mothers showed significant reductions in body weight and brain weight, cellularity, protein, cholesterol, cerebroside, and sulfatide contents. The reductions in wet brain weight and protein content were significant for cerebellum but not for cerebrum. Animals undernourished in utero and fed normally after birth showed normal whole brain weight, cerebroside and sulfatide contents, and normal cerebrum cellularity by adulthood. However, the type of cells increasing in the cerebrum during postnatal rehabilitation is unknown. Wet weight and cellularity were still diminished by 22% and 17%, respectively, in the adult cerebella. The results suggest that adequate postnatal nutrition will offset some, though not all of the brain biochemical changes resulting from fetal undernutrition.

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

Brain-to-body ratios and time of maturation of the mouse brain

1963 ◽  
Vol 204 (2) ◽  
pp. 343-346 ◽  
Author(s):  
Tsukasa Kobayashi
Keyword(s):  
Body Weight ◽  
Short Duration ◽  
Mouse Brain ◽  
Abrupt Change ◽  
Brain Weight ◽  
Second Phase ◽  
The Third ◽  
Third Phase ◽  
The Brain

Studies on the relationships of brain weight to body weight during development were conducted in 218 mice, and revealed three distinct phases. During the first phase, the ratios are relatively constant. The second phase of short duration is characterized by abrupt reductions. In the third phase, which is the most enduring, the ratios again assume more constant values. The abrupt change in the ratios took place around 14 days of age. It is suggested that the abrupt change in the ratio is, in general, an indicator of the maturation of the brain, because there are several other parameters which approach mature levels around the 15th day. A review of the data on other species supports this suggestion.

scholarly journals Walnut Oil Prevents Scopolamine-Induced Memory Dysfunction in a Mouse Model

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1630
Author(s):  
Jianqiao Liao ◽  
Yifan Nai ◽  
Li Feng ◽  
Yimeng Chen ◽  
Mei Li ◽  
...  
Keyword(s):  
Body Weight ◽  
Memory Impairment ◽  
Acetylcholinesterase Activity ◽  
Walnut Oil ◽  
Histological Changes ◽  
Hippocampal Ca1 ◽  
Malondialdehyde Content ◽  
Wet Weight ◽  
The Brain ◽  
Total Superoxide Dismutase

For thousands of years, it has been widely believed that walnut is a kind of nut that has benefits for the human body. Walnut oil, accounting for about 70% of walnut, mainly consists of polyunsaturated fatty acids. To investigate the effect of walnut oil on memory impairment in mice, scopolamine (3 mg/kg body weight/d) was used to establish the animal model during Morris Water Maze (MWM) tests. Walnut oil was administrated orally at 10 mL/kg body weight/d for 8 consecutive weeks. The results showed that walnut oil treatment ameliorated the behavior of the memory-impaired mice in the MWM test. Additionally, walnut oil obviously inhibited acetylcholinesterase activity (1.26 ± 0.12 U/mg prot) (p = 0.013) and increased choline acetyltransferase activity (129.75 ± 6.76 U/mg tissue wet weight) in the brains of scopolamine-treated mice (p = 0.024), suggesting that walnut oil could prevent cholinergic function damage in mice brains. Furthermore, walnut oil remarkably prevented the decrease in total superoxide dismutase activity (93.30 ± 5.50 U/mg prot) (p = 0.006) and glutathione content (110.45 ± 17.70 mg/g prot) (p = 0.047) and the increase of malondialdehyde content (13.79 ± 0.96 nmol/mg prot) (p = 0.001) in the brain of scopolamine-treated mice, indicating that walnut oil could inhibit oxidative stress in the brain of mice. Furthermore, walnut oil prevented histological changes of neurons in hippocampal CA1 and CA3 regions induced by scopolamine. These findings indicate that walnut oil could prevent memory impairment in mice, which might be a potential way for the prevention of memory dysfunctions.

scholarly journals Effects of pyridoxine deficiency and dl-p-chlorophenylalanine administration to rats on 5-hydroxytryptamine and noradrenaline concentrations in brain and 5-hydroxytryptamine concentration in blood

1973 ◽  
Vol 134 (3) ◽  
pp. 763-767 ◽  
Author(s):  
Hemmige N. Bhagavan ◽  
David B. Coursin
Keyword(s):  
Body Weight ◽  
Gastrointestinal Tract ◽  
Tryptophan Hydroxylase ◽  
Marked Decrease ◽  
Brain Weight ◽  
Pyridoxine Deficiency ◽  
Weanling Rats ◽  
And Control ◽  
Rate Limiting ◽  
The Brain

Pyridoxine deficiency in post-weanling rats caused a marked decrease in body weight and a small but significant decrease in brain weight. Although the concentration of circulating 5-hydroxytryptamine was markedly decreased, the concentrations of 5-hydroxytryptamine and noradrenaline in the brain were not affected. p-Chlorophenylalanine, an inhibitor of 5-hydroxytryptamine synthesis, decreased the 5-hydroxytryptamine content of brain to very low values in both the deficient and control animals, whereas the noradrenaline contents were not appreciably affected. The concentration of 5-hydroxytryptamine in blood, the origin of which is primarily gastrointestinal, was decreased only in the controls but not in the deficient animals after p-chlorophenylalanine treatment. These results suggest that whereas l-tryptophan hydroxylase (EC 1.14.3.2) is rate-limiting in the brain as has been reported by others, the pyridoxal 5′-phosphate-dependent enzyme 5-hydroxytryptophan decarboxylase (EC 4.1.1.28) may be more important in the gastrointestinal tract in the regulation of 5-hydroxytryptamine synthesis.

scholarly journals Histological study of the effects of aluminum chloride exposure on the brain of wistar rats female

2020 ◽  
Vol 10 (3-s) ◽  
pp. 37-42
Author(s):  
Hadjer Bekhedda ◽  
Norredine Menadi ◽  
Abbassia Demmouche ◽  
Abdelaziz Ghani ◽  
Hicham Mai
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Aluminum Chloride ◽  
Histological Study ◽  
The Body ◽  
Brain Weight ◽  
Female Rats ◽  
Aluminium Chloride ◽  
The Impact ◽  
The Brain

Introduction: Aluminum (Al) has the potential to be neurotoxic in human and animals, is present everywhere in the environment, many manufactured foods and medicines and is also added to drinking water for purification purposes and tooth paste cosmetic products They accumulate in living organisms and disrupt balances, and accumulate in the body biological systems, causing toxic effects (They may affect the nervous system, kidney, liver, respiratory or other functions). Nervous system is a vulnerable target for toxicants due to critical voltages which must be maintained in the cells and the all responses when voltages reach threshold levels. Objective This study aimed to expose the impact of aluminum chloride (AlCl3) on brain architecture. Methods: In our study, twenty healthy female rats were intraperitoneal administered of aluminum chloride (ALCL3) at 10 mg / kg body weight with consecutively for 15 day Result. The results showed a highly significant reduction in body weight (p<0.0001).  This is because aluminum has an anorectic effect contrariwise, there is no significant impact of aluminium exposure has been observed with respect to brain weight and relative brain weight respectively (p<0.912), (p<0.45). The histological study describes the alterations in the brain marked tissue necrosis and cytoplasmic vacuolations and karyopyknosis of neuronal cells of the brain. Conclusion; Aluminum is a toxic heavy metal and a ubiquitous environmental pollutant. It can alter the permeability of the blood-brain barrier and enter the brain, severely affecting the functioning of the nervous system. Keywords: Toxicity, brain, Aluminium chloride, Rats female, necrosis.

Body growth and carcass composition of lean reindeer (Rangifer tarandus tarandus L.) from birth to sexual maturity

1981 ◽  
Vol 59 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Tata M. Ringberg ◽  
Robert G. White ◽  
Dan F. Holleman ◽  
Jack R. Luick
Keyword(s):  
Body Weight ◽  
Rangifer Tarandus ◽  
Neonatal Period ◽  
Growth Period ◽  
Carcass Composition ◽  
Body Growth ◽  
Carcass Weight ◽  
Parotid Glands ◽  
Wet Weight ◽  
The Brain

Body growth and carcass composition were measured in lean reindeer during the juvenile growth period between birth and 3 years of age. Mean carcass weight in these lean reindeer was 56 ± 4% of body weight and the deposition of body muscle and bone mass was linearly correlated with body weight after the 1st month of age. The weight of the brain relative to body weight and carcass weight declined, while the relative changes in heart, liver, kidneys, parotid glands, and tissues of the gastrointestinal tract were small after the neonatal period. The extractable fat content in carcasses increased from 4.4 to 11.4% of wet weight or approximately 100 g fat at birth and 3.5 kg fat in adult reindeer. Fat-free dry matter represented a constant percentage (18–20%) of wet carcass weight independent of body weight after the neonatal period, while a significant inverse relationship between carcass fat and body water was found.

scholarly journals INDUKSI 2-METHOXYETHANOL PADA MASA PRENATAL SEBAGAI PENYEBAB KELAINAN OTAK PADA MENCIT

2004 ◽  
Vol 10 (1) ◽  
pp. 1-5
Author(s):  
Win Darmanto ◽  
Eko Prihiyantoro ◽  
Ria Harmonis
Keyword(s):  
Body Weight ◽  
Brain Development ◽  
Environmental Pollutants ◽  
Fetal Brain ◽  
Brain Weight ◽  
Total Weight ◽  
Control Group ◽  
Sterile Water ◽  
Cerebral Malformation ◽  
Pregnant Mice

2-Methoxyethanol (2-ME) and glycol esters are widely used as a solvents in the industry and plasticizers, and have becomes ubiquitous environmental pollutants. This study were designed to evaluate the malformation of brain development as an impact of 2-ME. Four groups of pregnant mice were injected to 2-ME dose 10 mmol/kg body weight at 7, 13, 15, and 17 days gestation respectively. Control group were injected with sterile water. At 18 days of gestation samples in groups 7 and 13 days gestation were sacrificed. Brain were remove and weight, morfologically and histologically were examined. Samples were divided into five groups, i.e. control group, 7th, 13rd, 15th and 17th days of gestation groups. Samples in 7th and 15th days of gestation groups killed in 18th days of gestation to observed fetal brain defect and decreased of fetal brain weight but some samples to allow delivery of fetuses. Furthermore, the fetuses killed on 0, 5, 10, and 20 days after birth, to take their brain. The result of these study showed that there are decreasing total weight of fetal brains and there are cerebral malformation as impact of 2-ME exposure.

Responses to cafeteria feeding in mice after the removal of interscapular brown adipose tissue

1982 ◽  
Vol 2 (11) ◽  
pp. 877-882 ◽  
Author(s):  
E. Connolly ◽  
J. A. Carnie
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Protein Content ◽  
Total Protein ◽  
Oxidase Activity ◽  
Total Protein Content ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Wet Weight

Feeding acafeteria diet to mice resulted in an increased energy intake of approximately 30% and this led to increases in the wet weight, total protein content, and total cytochrome oxidase activity of interscapular and dorso-cervical brown adipose tissue. Surgical removal of interscapular brown adipose tissue, followed by cafeteria feeding, gave rise to an elevation in dorso-cervical brown adipose tissue wet weight, total protein content, and total cytochrome oxidase activity, compared to intact cafeteria-fed mice. Cafeteria feeding with or without the removal of interscapular brown adipose tissue did not lead to significant increases in body weight compared to stock-fed control mice, but both cafeteria-fed groups of mice showed significant elevations in body fat content indicating that the induced hyperphagia led to a relative obesity in the cafeteria-fed groups. The results presented are consistent with an increased thermogenic activity in the brown adipose tissue of cafeteria-fed mice, and the effect of the removal of interscapular brown adipose tissue further indicates the quantitative importance of the tissue in the control of body weight.

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