An immunological study on the effect of brain extract on the developing nervous tissue in the chick embryo

Development ◽  
1964 ◽  
Vol 12 (1) ◽  
pp. 77-88
Author(s):  
D. J. McCallion ◽  
J. Langman
Keyword(s):  
Nervous Tissue ◽  
Brain Extract ◽  
Immunological Study ◽  
Chick Brain ◽  
Adult Chicken ◽  
Saline Extract ◽  
Chicken Brain ◽  
Tissue Extracts ◽  
Organ Systems ◽  
The Brain

In recent experiments 24–32 hr. chick embryos were treated with saline extract of adult chicken brain, which was injected into the yolk, into the sub-blastodermal space, or deposited over the blastoderm. After an additional 60-hr, incubation period, 30 to 40 per cent of the surviving embryos showed defects of the brain, spinal cord and eye, such as anencephalus, microcephalus, abnormal shape of the brain vesicles, rachischisis, anophthalmia and microphthalmia (Lenicque, 1959; Clarke & McCallion, 1959; Braverman, 1961). In addition, a number of embryos showed abnormal proliferation in the walls of the brain vesicles. When other tissue extracts were examined it was found that the abovementioned abnormalities could be produced only by saline extracts of chick brain and nervous retina, and not by extracts prepared from liver, spleen and skeletal muscle. The latter extracts do sometimes affect brain development, but then always in association with defects in other organ systems.

Effects of brain extracts on activity of the trigeminal motor and hypoglossal nuclei

1961 ◽  
Vol 201 (2) ◽  
pp. 341-346
Author(s):  
Yojiro Kawamura ◽  
Masaya Funakoshi ◽  
Mitsuru Takata
Keyword(s):  
Brain Tissue ◽  
Ethanol Extract ◽  
Tris Buffer ◽  
Brain Extract ◽  
Cortical Tissue ◽  
Saline Extract ◽  
Tissue Extracts ◽  
Lower Jaw ◽  
Brain Extracts ◽  
The Brain

Alterations in trigeminal motor and hypoglossal nuclei discharges were noted following microinjections of ethanol and saline brain tissue extracts, ACh and γ-aminobutyric acid (GABA). Background activities of these nuclei were not affected by microinjection of 0.9% saline solution or tris buffer [tris (hydroxymethyl) amino methane] of pH 7.2. Solutions of pH 8.5 (tris buffer) or pH 5.8 (glycine buffer) gradually inhibited these discharges. Spontaneous discharges of the trigeminal motor nuclei were accelerated by the saline extract of the brain tissue and ACh, and they were inhibited by the ethanol extract of the brain tissue and GABA. Discharge of this nucleus accelerated by lower jaw depression was also inhibited by the ethanol brain extract and GABA. Background activity of the hypoglossal nuclei was mildly accelerated by the saline brain extracts and ACh, greatly accelerated by the ethanol brain extracts, and strongly inhibited by GABA. The saline extract of the brain tissue extracted from brain stem had a stronger activator than that extracted from cortical tissue.

Transient embryonic antigens in the chick

Development ◽  
1964 ◽  
Vol 12 (3) ◽  
pp. 511-516
Author(s):  
D. J. McCallion ◽  
J. C. Trott
Keyword(s):  
Spinal Cord ◽  
Chick Embryo ◽  
Primitive Streak ◽  
Adult Chicken ◽  
Tissue Specific ◽  
Chicken Brain ◽  
Early Chick Embryo ◽  
Embryonic Antigens ◽  
Specific Antigens ◽  
The Brain

The Presence of an organ antigen in the early chick embryo was first demonstrated by Schechtman (1948). He found that an antigenic substance common to brain, heart, liver and muscle of chicks at hatching is already present in primitive streak and early neurula stages of the embryo. This observation, with respect to brain and heart, was subsequently confirmed by Ebert (1950). McCallion & Langman (1964) have recently demonstrated that there are at least eight antigenic substances in the adult chicken brain that are class-specific but that are more or less common to other organs, with only quantitative differences. These authors have further demonstrated that there are at least three, possibly as many as five, antigenic substances in adult chicken brain that are not only class-specific but also tissue-specific, occurring only in the brain, spinal cord, nervous retina and nerves. The non-specific antigens appear progressively during the first 4 days of incubation.

scholarly journals Ontogenic Redistribution of Type 2 Deiodinase Messenger Ribonucleic Acid in the Brain of Chicken

Endocrinology ◽  
2004 ◽  
Vol 145 (8) ◽  
pp. 3619-3625 ◽  
Author(s):  
Balázs Gereben ◽  
Janusz Pachucki ◽  
Anna Kollár ◽  
Zsolt Liposits ◽  
Csaba Fekete
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Hormone Receptors ◽  
Third Ventricle ◽  
Hybridization Signal ◽  
Adult Chicken ◽  
Chicken Brain ◽  
Messenger Ribonucleic Acid ◽  
The Brain

Abstract Thyroid hormone is essential for brain development. T4 has to be converted to T3 for efficient binding to thyroid hormone receptors. Type 2 deiodinase (D2) is the key enzyme that allows T3 generation in the brain. To elucidate the onset and localization of T3 production in the brain, we studied the changes of D2 activity, mRNA content, and the distribution of D2 mRNA in the brain of chicken embryos before and after the onset of thyroid function. D2 activity was detectable in the brain at all stages studied from embryonic day (E)7 to E15 and increased significantly with time. The wild-type chicken D2 transcript was detectable at all those stages by RT-PCR. The amount of D2 mRNA in the brain increased approximately 14-fold from E10 to E17 as assessed by Northern blot. Week D2 hybridization signal could be detected by in situ hybridization at E8 in cell clusters throughout the brain, and its intensity markedly increased to E15. Interestingly, no D2 expression was detected in hypothalamic tanycytes at these embryonic stages. However, D2 hybridization signal was observed in the wall of the third ventricle of adult chicken posterior to the rostral pole of the median eminence in the location typical for tanycytes, whereas D2 signal in other localizations was decreased throughout the brain. Our data suggest that D2 contributes to T3 content of the developing chicken brain even before the onset of thyroid function. Furthermore, redistribution of D2 mRNA expression was observed during the development of the chicken brain.

scholarly journals Cytomegalovirus Infection and Inflammation in Developing Brain

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1078
Author(s):  
Fran Krstanović ◽  
William J. Britt ◽  
Stipan Jonjić ◽  
Ilija Brizić
Keyword(s):  
Cytomegalovirus Infection ◽  
Hcmv Infection ◽  
Severe Disease ◽  
Intraperitoneal Administration ◽  
Inflammatory Factors ◽  
Mcmv Infection ◽  
Newborn Mice ◽  
Organ Systems ◽  
Congenital Hcmv Infection ◽  
The Brain

Human cytomegalovirus (HCMV) is a highly prevalent herpesvirus that can cause severe disease in immunocompromised individuals and immunologically immature fetuses and newborns. Most infected newborns are able to resolve the infection without developing sequelae. However, in severe cases, congenital HCMV infection can result in life-threatening pathologies and permanent damage of organ systems that possess a low regenerative capacity. Despite the severity of the problem, HCMV infection of the central nervous system (CNS) remains inadequately characterized to date. Cytomegaloviruses (CMVs) show strict species specificity, limiting the use of HCMV in experimental animals. Infection following intraperitoneal administration of mouse cytomegalovirus (MCMV) into newborn mice efficiently recapitulates many aspects of congenital HCMV infection in CNS. Upon entering the CNS, CMV targets all resident brain cells, consequently leading to the development of widespread histopathology and inflammation. Effector functions from both resident cells and infiltrating immune cells efficiently resolve acute MCMV infection in the CNS. However, host-mediated inflammatory factors can also mediate the development of immunopathologies during CMV infection of the brain. Here, we provide an overview of the cytomegalovirus infection in the brain, local immune response to infection, and mechanisms leading to CNS sequelae.

scholarly journals FOXP1 syndrome: a review of the literature and practice parameters for medical assessment and monitoring

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Reymundo Lozano ◽  
Catherine Gbekie ◽  
Paige M. Siper ◽  
Shubhika Srivastava ◽  
Jeffrey M. Saland ◽  
...  
Keyword(s):  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Medical Assessment ◽  
Forkhead Box ◽  
Organ Systems ◽  
Practice Parameters ◽  
Assessment And Monitoring ◽  
Multidisciplinary Group ◽  
The Brain

AbstractFOXP1 syndrome is a neurodevelopmental disorder caused by mutations or deletions that disrupt the forkhead box protein 1 (FOXP1) gene, which encodes a transcription factor important for the early development of many organ systems, including the brain. Numerous clinical studies have elucidated the role of FOXP1 in neurodevelopment and have characterized a phenotype. FOXP1 syndrome is associated with intellectual disability, language deficits, autism spectrum disorder, hypotonia, and congenital anomalies, including mild dysmorphic features, and brain, cardiac, and urogenital abnormalities. Here, we present a review of human studies summarizing the clinical features of individuals with FOXP1 syndrome and enlist a multidisciplinary group of clinicians (pediatrics, genetics, psychiatry, neurology, cardiology, endocrinology, nephrology, and psychology) to provide recommendations for the assessment of FOXP1 syndrome.

THE HYDROLYSIS OF MONOPHOSPHOINOSITIDE BY EXTRACTS OF BRAIN

1967 ◽  
Vol 45 (6) ◽  
pp. 853-861 ◽  
Author(s):  
W. Thompson
Keyword(s):  
Fatty Acids ◽  
Enzyme Activity ◽  
Calcium Ions ◽  
Brain Extract ◽  
Monovalent Cations ◽  
High Concentration ◽  
Diffusible Factor ◽  
Hydrolysis Of ◽  
The Brain ◽  
Long Chain

The hydrolysis of monophosphoinositide by soluble extracts from rat brain is described. Diglyceride and inositol monophosphate are liberated along with a small amount of free fatty acids. Hydrolysis of the lipid is optimal at pH 5.4 in acetate buffer. The reaction is stimulated by calcium ions or by high concentration of monovalent cations and, to a less extent, by long-chain cationic amphipathic compounds. Enzyme activity is lost on dialysis of the brain extract and can be restored by diffusible factor(s). Some differences in the conditions for hydrolysis of mono- and tri-phosphoinositides are noted.

CRYPTIC CAUSES AND MECHANISMS INVOLVED IN AGEING

INDIAN DRUGS ◽  
2013 ◽  
Vol 50 (01) ◽  
pp. 5-22
Author(s):  
K Challabotla ◽  
◽  
D Banji ◽  
O.J.F Banji ◽  
Chilipi K Reddy
Keyword(s):  
Oxidative Stress ◽  
Developing Countries ◽  
Molecular Basis ◽  
Metabolic Disorders ◽  
Natural Process ◽  
Biological Functions ◽  
Stress Theory ◽  
Biochemical Alterations ◽  
Organ Systems ◽  
The Brain

Ageing is a natural process characterized by progressive deterioration of biological functions. Ageing causes both morphological as well as biochemical alterations in various body organs leading to deterioration of health. Proteins, enzymes and neurotransmitters are affected, which in turn can result in dysregulation of various pathways. WHO has reported that by 2020, three quarters of all deaths in developing countries will be age-associated. Currently more than 300 theories exist to explain the phenomenon of ageing; amongst them the oxidative stress theory of ageing is most studied and accepted for the molecular basis of ageing. All these processes can progress at an unprecedented pace on contact with triggering factors, leading to the development of pathological ageing. The probability of developing neurodegenerative and metabolic disorders is relatively high under such circumstances. This review emphasizes the theories and mechanisms of ageing and an overview on the aspects of age associated biochemical changes and the implications on the brain, liver and various organ systems.

scholarly journals Sources: The Brain, the Nervous System, and Their Diseases

2015 ◽  
Vol 54 (4) ◽  
pp. 79 ◽  
Author(s):  
Maria C. Melssen
Keyword(s):  
Nervous System ◽  
Organ Systems ◽  
The Brain

Jenniefer L. Hellier's The Brain, the Nervous System, and Their Diseases fulfills its purpose as a single, comprehensive resource that covers all aspects of the brain, nervous system, and the diseases effecting these organ systems. The text is easy to navigate: entries are listed alphabetically and by topic. A detailed index is also provided at the end of volume 3. The 333 entries vary in length from several paragraphs to multiple pages and include "see also" references and lists of further readings. Images, tables, charts, and graphs are provided when available. A list of recommended resources at the end of the encyclopedia provides only eight resources; however, each entry's own list of further readings makes up for the brevity of this list.

scholarly journals Is mercury injected into the body for therapeutic purposes released into the spinal fluid?

1912 ◽  
Vol XIX (4) ◽  
pp. 803-813
Author(s):  
V. Lazarev
Keyword(s):  
Tuberculous Meningitis ◽  
Nervous Tissue ◽  
Direct Action ◽  
The Body ◽  
Spinal Fluid ◽  
Bile Pigment ◽  
Vascular Plexus ◽  
Points Of View ◽  
The Brain ◽  
Theoretical Side

Is mercury injected into the body excreted into the spinal fluid? This question occupied us with practical and theoretical points of view. On the practical side, we were interested in knowing how much we can count on the circulation of mercury in the spinal fluid and, therefore, on its direct action on the nervous tissue due to the communication of the perivascular (and pericellular) spaces with the sub-arachnoid. If mercury is released into the spinal fluid, it is necessary to search for the therapeutic effect (syphilis of the nervous system) of the drug that quickly and in large quantities passes into the spinal fluid. On the theoretical side, the issue of mercury release is of interest for solving the broader issue of the nature of spinal fluid in general. As is known, there is currently no agreement on this account. Is the spinal fluid transudate, the secretion of the vascular plexus epithelium or the sui generis lymph of the brain itself. In favor of the second1 views are inclined by Schultze, Imamura, Raubitschek, Molt, and others in favor of the last but Spina2 (also Lewandovsky and Blumenthal3. The first view is generally accepted. We thought that the saturation of blood with mercury, which happens with prolonged introduction of it into the body, should lead to the appearance of at least traces of it in the spinal fluid, if the latter is transudate. If the last secret, then apriori nothing can be predicted; extraction depends on the chemical and physical properties of the epithelium itself; the epithelium can secerne one substance and not pass another. The number of substances found so far in the spinal fluid when injected into the body is very limited. When the brain (and membranes) was normal, the substances introduced by the authors did not completely enter the spinal fluid. Widal, Monod4, Sicard was found in tuberculous meningitis iod when giving it during 2-3 days for 3-5 grams only in 3 cases. Guinon and Simon found only 1/2 cases of tuberculous meningitis; no iodine was found in cases of cerebrospinal meningitis. With uremia, Costaigne found iod and methylene blue. Sicard and Widal didnt find it. Gilbert and Castaigne found bile pigment in jaundice. Sicard denies. Archard Loeper5 did not find the lithium when it was injected into the blood. Regarding the fate of mercury introduced into the organism, there are no indications in the literature6.

Abstract WP265: Interferon-inducible Protein 10 Increases following Stroke

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Hilary A Seifert ◽  
Lisa A Collier ◽  
Stanley A Benkovic ◽  
Alison E Willing ◽  
Keith R Pennypacker
Keyword(s):  
Time Course ◽  
Neutralizing Antibody ◽  
Artery Occlusion ◽  
T Helper ◽  
Protein Levels ◽  
Organ Systems ◽  
Inducible Protein ◽  
Cerebral Artery Occlusion ◽  
The Brain ◽  
Interferon Inducible Protein

Objective: The splenic response to injury furthers cellular degeneration as its removal is protective in ischemic injuries to several organ systems including the brain. Previously, we have shown that the proinflammatory cytokine interferon gamma (IFNg), which activates microglia/macrophages, is elevated in the spleen and the brain following permanent middle cerebral artery occlusion (MCAO). IFNg induces the production of interferon-inducible protein 10 (IP-10) which further propagates the inflammatory response. Therefore, we investigated the expression of IP-10 in the brain and spleen following ischemic stroke. Hypothesis: IFNg production in the brain and the spleen results in elevated levels of IP-10 in the same tissues post-MCAO. Methods: A time course was conducted to investigate splenic and brain protein levels of IP-10 in rats over time following MCAO and sham-MCAO (n≥3). In a second experiment, rats were administered an IFNg neutralizing antibody following MCAO with a survival time of 96 h: vehicle control (n=4), goat IgG 5μg (n=7), and IFNg antibody 5μg (n=7). Spleens and brains were collected for all groups. Results: IP-10 levels were significantly elevated in the brain at 72 and 96 h post-MCAO (p<0.01) compared to naïve brains. In the spleen IP-10 levels become significantly elevated at 24 h and remain elevated out to 96 h post-MCAO (p<0.0007) compared to naïve spleens. Administration of a neutralizing antibody directed against IFNg significantly decreased IP-10 levels in the brain (p<0.009) but did not affect IP-10 levels in the spleen. Conclusion: These results demonstrate that increased production of IFNg results in elevated levels of IP-10 in both the spleen and the brain following stroke. However, administration of a neutralizing antibody against IFNg decreased the amount of IP-10 in the brain. Levels of IFNg and IP-10 in the brain increase at the same time following stroke. Based on these data, IFNg propagates a proinflammatory T helper cell response to stroke through IP-10. Inhibition of this signaling could reduce neuroinflammation thereby improving stroke outcome.

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