NUTRITION, GROWTH AND NEUROINTEGRATIVE DEVELOPMENT: AN EXPERIMENTAL AND ECOLOGIC STUDY

PEDIATRICS ◽  
1966 ◽  
Vol 38 (2) ◽  
pp. 319-320 ◽  
Author(s):  
Joaquin Cravioto ◽  
Elsa R. DeLicardie ◽  
Herbert G. Birch
Keyword(s):  
Nervous System ◽  
Animal Experiments ◽  
Ecologic Study ◽  
Large Pool ◽  
Environmental Responsiveness ◽  
Social Custom ◽  
The Central Nervous System ◽  
Physical Stature ◽  
Inadequate Food Intake ◽  
Normal Controls

IN THIS MONOGRAPH we report the results of an experimental and ecologic study concerned with estimating some of the effects which malnutrition in early childhood may have upon neurointegrative functioning. In particular, we have been concerned with the association between malnutrition early in childhood and intersensory organization in children during the school years. A study of these relationships has derived from a concern with the possibility that inadequate food intake, particularly as represented by protein-calorie malnutrition, affects not only stature and weight, but also the capacity to learn. If this is indeed the case, then the significance of the observable and dramatic consequences of malnutrition for physical stature may be but one visible sign of functionally, perhaps, far more important non-visible handicapping. Findings on the effects which malnutrition has on the central nervous system suggest strongly that protein deficiency may result in structural lesions of the nervous system. Animals experimentally deprived are persistently delayed in achieving simple developmental landmarks, appear to be less adequate in environmental responsiveness and slower in learning as well as poorer in the retention of that which has been learned than normal controls. Considering the animal experiments and the findings in humans as a unit, one is led to be concerned with what in an ecologic sense could be called a "spiral" effect. A low level of adaptive capacity, ignorance, social custom, infection, or environmental paucity of foodstuffs appear to result in malnutrition which may produce a large pool of individuals who come to function in suboptimal ways.

scholarly journals Hormonal imprinting in the central nervous system: causes and consequences

2013 ◽  
Vol 154 (4) ◽  
pp. 128-135 ◽  
Author(s):  
György Csaba
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Environmental Pollutants ◽  
Methylation Pattern ◽  
Critical Periods ◽  
Hormonal Imprinting ◽  
Modern Age ◽  
The Central Nervous System

The notion of the perinatal „hormonal imprinting” has been published at first in 1980 and since that time it spred expansively. The imprintig develops at the first encounter between the developing receptor and the target hormone – possibly by the alteration of the methylation pattern of DNA – and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor’s binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably influences the dopaminergic, serotonergic and noradrenergic system and this can be manifested – in animal experiments – in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the mass of medicaments, chemicals, the presence of hormone-like materials (e.g. soya phytosteroids) in the food, and environmental pollutants. The author especially emphasizes the danger of oxytocin, as a perinatal imprinter, as it is used very broadly and can basically influence the emotional and social spheres and the appearance of certain diseases such as auitism, schizophrenia and parkinsonism. The danger of perinatal imprinters is growing, considering their effects on the human evolution. Orv. Hetil., 2013, 154, 128–135.

scholarly journals THE ROLE OF MAGNESIUM DEFICIENCY AND ITS SUPPLEMATION IN DISEASES OF CENTRAL NERVOUS SYSTEM. REVIEW

2018 ◽  
Vol 13 (3-4) ◽  
pp. 70-75
Author(s):  
M.V. Khaitovych
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Magnesium Deficiency ◽  
Close Association ◽  
Animal Experiments ◽  
Depression And Anxiety ◽  
Literary Sources ◽  
The Central Nervous System ◽  
System Review

Relevance. Anti-depressant effects of NMDA receptor antagonists have been proven, a close association between low levels of magnesium in the blood and depression. Therefore, in recent years, antidepressant properties of magnesium are actively studied in animal experiments. Objective: To review modern literary sources about the role of magnesium deficiency in the pathogenesis of diseases of the central nervous system. Materials and methods. Searching for a depth of 12 years at Scopus, Google Scholar. Results. The results of experimental and clinical researches pointed out on association between low level of magnesium in hair, liquor, brain with higher risk of development dementia, depression and anxiety. An additional supplementation with magnesium in patients associates with decreasing risk of ischemic stroke and dementia, in pregnancy – provides neuroprotection of fetus, in case of depression increases effectiveness of antidepressants, in brain injury associates with faster recovery of cognitive functions, in migraines - with decreasing in the frequency of attacks and improvement of the quality patients’ lives, in case of neuroleptic therapy - with the possibility of delayed appearance or absence of manifestations of drug parkinsonism. These changes are explained by antagonistic effects of magnesium on glutamate receptors, decreasing oxidative stress intensity as well as neural cell  apoptosis. Conclusion. Magnesium plays an important neuroprotective role.

THE SPIDER NEVUS IN INFANCY AND CHILDHOOD

PEDIATRICS ◽  
1964 ◽  
Vol 33 (2) ◽  
pp. 227-232
Author(s):  
James E. Wenzl ◽  
E. Omer Burgert
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Illnesses ◽  
Healthy Children ◽  
Normal Children ◽  
Infancy And Childhood ◽  
Spider Nevus ◽  
The Central Nervous System ◽  
Anatomic Distribution ◽  
Normal Controls

At the Mayo Clinic 711 children, ranging in age from birth to 15 years, were examined for the presence of spider nevi. The children were divided into three groups: normal controls, patients with chronic illness and patients with disease of the central nervous system. In the normal children, the incidence of spider nevi increased rapidly after 2 years of age to reach a plateau at about the time of puberty for both sexes. In children more than 13 years of age the incidence appeared to be decreasing, presumably toward the stated incidence of 12 to 15% in so-called normal adults. In normal children, spider nevi appeared to occur more frequently in pubertal females than in pubertal males. The incidence was increased in both sexes in patients more than 4 years of age with disease of the central nervous system. In patients with chronic illnesses, there was no significant increase in spider nevi, but the ratio of pubertal females to pubertal males was reversed. The anatomic distribution in all groups differed from that of adults, the dorsum of the hands and forearms being the sites of predilection in children. In view of the frequency of these lesions in childhood, it appears that the presence of spider nevi in otherwise healthy children is an insignificant stigma.

Dystrophin and dystrophin-related protein in the central nervous system of normal controls and Duchenne muscular dystrophy

1994 ◽  
Vol 87 (2) ◽  
pp. 129-134 ◽  
Author(s):  
Makoto Uchino ◽  
Hitoo Teramoto ◽  
Hiroaki Naoe ◽  
Teruhisa Miike ◽  
Kowashi Yoshioka ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Related Protein ◽  
The Central Nervous System ◽  
Normal Controls

A Clinical Trial with a New Anticonvulsant Drug, α-(P-Aminophenyl)-α-Ethyl Glutarimide Preparation 16038 (Ciba)

1959 ◽  
Vol 105 (439) ◽  
pp. 448-456 ◽  
Author(s):  
Walter Fabisch
Keyword(s):  
Clinical Trial ◽  
Central Nervous System ◽  
Nervous System ◽  
Animal Experiments ◽  
Anticonvulsant Drug ◽  
The Central Nervous System ◽  
Derivatives Of

Derivatives of glutarimide are known to exert an effect upon the central nervous system. To name only two which are widely used for clinical purposes: Glutethimide (“Doriden”) is a sedative, Bemigride (“Megimide”) a stimulant. Preparation 16038 (Ciba) α-(p-aminophenyl)-α-ethyl glutarimide, in animal experiments had shown properties which suggested its use as an anticonvulsant, and this paper is an account of a clinical trial with the substance on in- and out-patients suffering from epilepsy.

Population screening for association of mitochondrial haplogroups BM, J, K and M with multiple sclerosis: interrelation between haplogroup J and MS in Persian patients

2005 ◽  
Vol 11 (6) ◽  
pp. 728-730 ◽  
Author(s):  
M Houshmand ◽  
M H Sanati ◽  
F Babrzadeh ◽  
A Ardalan ◽  
M Teimori ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Young Adults ◽  
Mitochondrial Dna ◽  
Mitochondrial Haplogroups ◽  
Mtdna Mutations ◽  
Pcr Rflp ◽  
The Central Nervous System ◽  
Normal Controls

Background: Multiple sclerosis (MS) is an immunological inflammatory disease of the central nervous system (CNS) which is chronically observed in young adults. On the basis of earlier studies, potential relatedness between MS and mitochondrial DNA (mtDNA) mutations was postulated. Materials and methods: 246 individuals were screened using the PCR-RFLP method, including 70 MS patients examined for mitochondrial haplogroups BM, J, K and M and 176, 149 and 70 normal controls examined for haplogroups BM and M, J and K, respectively. Results and discussion: Our analysis revealed a relatively high proportion of haplogroup BM in MS patients (∼26%) compared to normal controls (∼13%). In addition, a slightly significant increase of MS patients of haplogroup J (20% in MS patients versus 9.39% in normal controls at P-0.049), while haplogroups M and K did not show contribution to MS contingency (2.85 and 2.27%, respectively at P-1.000 in haplogroup M and 12.85 and 7.14% respectively at P-0.399 in haplogroup K).

scholarly journals Biochemical and Structural Characteristics, Gene Regulation, Physiological, Pathological and Clinical Features of Lipocalin-Type Prostaglandin D2 Synthase as a Multifunctional Lipocalin

2021 ◽  
Vol 12 ◽  
Author(s):  
Yoshihiro Urade
Keyword(s):  
Nervous System ◽  
Structural Characteristics ◽  
Animal Experiments ◽  
Amyloid Β ◽  
Future Research ◽  
Prostaglandin D2 ◽  
Major Protein ◽  
Common Precursor ◽  
Pathophysiological Role ◽  
The Central Nervous System

Lipocalin-type prostaglandin (PG) D2 synthase (L-PGDS) catalyzes the isomerization of PGH2, a common precursor of the two series of PGs, to produce PGD2. PGD2 stimulates three distinct types of G protein-coupled receptors: (1) D type of prostanoid (DP) receptors involved in the regulation of sleep, pain, food intake, and others; (2) chemoattractant receptor-homologous molecule expressed on T helper type 2 cells (CRTH2) receptors, in myelination of peripheral nervous system, adipocyte differentiation, inhibition of hair follicle neogenesis, and others; and (3) F type of prostanoid (FP) receptors, in dexamethasone-induced cardioprotection. L-PGDS is the same protein as β-trace, a major protein in human cerebrospinal fluid (CSF). L-PGDS exists in the central nervous system and male genital organs of various mammals, and human heart; and is secreted into the CSF, seminal plasma, and plasma, respectively. L-PGDS binds retinoic acids and retinal with high affinities (Kd < 100 nM) and diverse small lipophilic substances, such as thyroids, gangliosides, bilirubin and biliverdin, heme, NAD(P)H, and PGD2, acting as an extracellular carrier of these substances. L-PGDS also binds amyloid β peptides, prevents their fibril formation, and disaggregates amyloid β fibrils, acting as a major amyloid β chaperone in human CSF. Here, I summarize the recent progress of the research on PGD2 and L-PGDS, in terms of its “molecular properties,” “cell culture studies,” “animal experiments,” and “clinical studies,” all of which should help to understand the pathophysiological role of L-PGDS and inspire the future research of this multifunctional lipocalin.

Dystrophin and dystrophin-related protein in the central nervous system of normal controls and Duchenne muscular dystrophy

1994 ◽  
Vol 87 (2) ◽  
pp. 129-134 ◽  
Author(s):  
Makoto Uchino ◽  
Hitoo Teramoto ◽  
Hiroaki Naoe ◽  
Teruhisa Miike ◽  
Kowashi Yoshioka ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Related Protein ◽  
The Central Nervous System ◽  
Normal Controls
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