An Alternative Amino-Terminus Expressed in the Central Nervous System Converts Agrin to a Type II Transmembrane Protein

2001 ◽  
Vol 17 (1) ◽  
pp. 208-225 ◽  
Author(s):  
Frank R. Neumann ◽  
Godela Bittcher ◽  
Maik Annies ◽  
Beat Schumacher ◽  
Stephan Kröger ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transmembrane Protein ◽  
Amino Terminus ◽  
Type Ii ◽  
The Central Nervous System

scholarly journals Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleotide Metabolism ◽  
Neural Cells ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Neuroepithelial Cells ◽  
The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

Mucopolysaccharidosis in Adults

2016 ◽  
Author(s):  
Christian J. Hendriksz ◽  
Francois Karstens
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Autosomal Recessive ◽  
Clinical Symptoms ◽  
Cell Types ◽  
Type Ii ◽  
System P ◽  
Different Types ◽  
The Central Nervous System ◽  
Different Cell Types

There are 8 different types of diseases of the mucopolysaccharides, each caused by a deficiency in one of 10 different enzymes involved in the degradation of glycosaminoglycans (GAGs). Partially degraded GAGs accumulate within the lysosomes of many different cell types and lead to clinical symptoms and excretion of large amounts of GAGs in the urine. Heritability is autosomal recessive except for MPS type II, which is X-linked. The disorders are chronic and progressive and, although the specific types all have their individual features, they share an abundance of clinical similarities. All involve the musculoskeletal, the cardiovascular, the pulmonary and the central nervous system.

scholarly journals Endothelial Expression of TGFβ Type II Receptor Is Required to Maintain Vascular Integrity during Postnatal Development of the Central Nervous System

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39336 ◽  
Author(s):  
Kathleen R. Allinson ◽  
Hye Shin Lee ◽  
Marcus Fruttiger ◽  
Joseph McCarty ◽  
Helen M. Arthur
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Postnatal Development ◽  
Type Ii ◽  
Vascular Integrity ◽  
The Central Nervous System

scholarly journals ARNOLD-CHIARI MALFORMATION: LITERATURE REVIEW AND CLINICAL CASE IN SIBLINGS

2021 ◽  
Vol 11 (1(39)) ◽  
pp. 58-64
Author(s):  
Anastasiya Babintseva ◽  
Yu.Yu. Khodzinska ◽  
І.V. Lastivka ◽  
О.І. Yurkiv ◽  
A.I. Roshka ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chiari Malformation ◽  
Clinical Case ◽  
Type Ii ◽  
Hernia Sac ◽  
Arnold Chiari Malformation ◽  
System Type ◽  
The Central Nervous System ◽  
The Brain

Arnold-Chiari malformation is a defectof the cervical-medullar transition characterized bydisplacement of the cerebellar tonsils and in a numberof cases when the stem and IV ventricle extend into theforamen magnum. There are four main types of pathology,and type II is found most often.The article presents a clinical case of type II ArnoldChiari malformation in siblings. The newborn girl born afterVII pregnancy and VII physiological delivery in the termof 39-40 weeks was under observation. US examination inthe terms of 20-21 and 34 weeks of gestation diagnoseda congenital developmental defect of the central nervoussystem characterized by a “lemon”-like shape of the brain,displacement of the brain structures in the portion of theforamen magnum, ventriculomegaly, a defect of the lumbarsacral portion with formation of hernia sac, and dropsy ofamnion. The family couple refused from interruption ofpregnancy and medical-genetic examination.The basic diagnosis of the child was congenitaldevelopmental defect of the central nervous system(type II Arnold-Chiari malformation: rachischisis andhydrocephalus) including complications such as inferiortorpid paraplegia and dysfunction of the pelvic organs.Investigation of hereditary anamnesis foundcompromised heredity on the mother’s side (her mother’ssibling has Down’s syndrome), and IV child in the familyis disabled from birth due to a congenital developmentaldefect of the central nervous system – type II Arnold-Chiarimalformation.The family couple refused from a comprehensivemedical-genetic consultation during the previous andcurrent pregnancies, and magnetic-resonance imaging ofthe child.

scholarly journals Toxoplasma gondii Infections Alter GABAergic Synapses and Signaling in the Central Nervous System

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Justin M. Brooks ◽  
Gabriela L. Carrillo ◽  
Jianmin Su ◽  
David S. Lindsay ◽  
Michael A. Fox ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Toxoplasma Gondii ◽  
Acid Decarboxylase ◽  
Global Changes ◽  
Type Ii ◽  
Content Type ◽  
Gabaergic Synapses ◽  
The Central Nervous System ◽  
The Brain

ABSTRACTDuring infections with the protozoan parasiteToxoplasma gondii, gamma-aminobutyric acid (GABA) is utilized as a carbon source for parasite metabolism and also to facilitate parasite dissemination by stimulating dendritic-cell motility. The best-recognized function for GABA, however, is its role in the nervous system as an inhibitory neurotransmitter that regulates the flow and timing of excitatory neurotransmission. When this pathway is altered, seizures develop. Human toxoplasmosis patients suffer from seizures, suggesting thatToxoplasmainterferes with GABA signaling in the brain. Here, we show that while excitatory glutamatergic presynaptic proteins appeared normal, infection with type II ME49Toxoplasmatissue cysts led to global changes in the distribution of glutamic acid decarboxylase 67 (GAD67), a key enzyme that catalyzes GABA synthesis in the brain. Alterations in GAD67 staining were not due to decreased expression but rather to a change from GAD67 clustering at presynaptic termini to a more diffuse localization throughout the neuropil. Consistent with a loss of GAD67 from the synaptic terminals,Toxoplasma-infected mice develop spontaneous seizures and are more susceptible to drugs that induce seizures by antagonizing GABA receptors. Interestingly, GABAergic protein mislocalization and the response to seizure-inducing drugs were observed in mice infected with type II ME49 but not type III CEP strain parasites, indicating a role for a polymorphic parasite factor(s) in regulating GABAergic synapses. Taken together, these data support a model in which seizures and other neurological complications seen inToxoplasma-infected individuals are due, at least in part, to changes in GABAergic signaling.IMPORTANCEInfections of the central nervous system can cause seizures. While inflammation in the brain has been proposed to initiate the onset of the seizures, relatively little is known about how inflammation impacts the structure and function of the neurons. Here we used a parasite calledToxoplasma gondiithat infects the brain and showed that seizures arise due to a defect in signaling of GABA, which is the neurotransmitter primarily responsible for preventing the onset of seizures.

scholarly journals Development of thyroxine type II deiodinase activity in brains of Zucker rats

1994 ◽  
Vol 304 (1) ◽  
pp. 259-261 ◽  
Author(s):  
V Marie ◽  
F Dupuy ◽  
R Bazin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Zucker Rats ◽  
Early Event ◽  
Type Ii ◽  
Free T4 ◽  
Serum Free ◽  
Obese Rats ◽  
The Central Nervous System ◽  
T4 Conversion

The present study was undertaken to determine whether the capacity for 3,5,3′,5′-tetraiodothyronine (T4) conversion into 3,5,3′-tri-iodothyronine (T3), as measured by the activity of thyroxine type II 5′-monodeiodinase (T4-5′D), was altered in the brains of young Zucker fa/fa rats during the period of intense maturation of the central nervous system (i.e. from 10 to 20 days of life). From 7 to 14 days of age, no difference in brain T4-5′D activity could be detected between lean and pre-obese rats; serum free T4 was not affected by the fa gene. During the suckling to weaning transition, T4-5′D reached a plateau in brains of lean rats, while it increased by 50% in brains of pre-obese rats; concurrently, serum free T4 increased in Fa/fa rats, whereas it did not change in fa/fa rats. The increased capacity for conversion of T4 into T3 observed in brains of pre-obese compared with lean rats could not be ascribed to a variation in the amount of T4-5′D, since Vmax. did not differ between the two genotypes; however, it could be totally accounted for by an increased affinity of the enzyme for T4. This change may represent an adaptive response to low serum free T4 in order to maintain the cerebral T3 concentration in pre-obese rats. These results show that the alteration in T4 metabolism in brains of fa/fa rats is not an early event and thus cannot interfere with maturation of the central nervous system. However, the decreased serum free T4 which was observed in pre-obese rats after suckling might play a secondary role in development of this genetic obesity.

AAV9 mediated correction of iduronate-2-sulfatase deficiency in the central nervous system of mucopolysaccharidosis type II mice

2016 ◽  
Vol 117 (2) ◽  
pp. S70
Author(s):  
Kanut Laoharawee ◽  
Kelly M. Podetz-Petersen ◽  
Kelley F. Kitto ◽  
Lucy Vulchanova ◽  
Carolyn A. Fairbanks ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mucopolysaccharidosis Type ◽  
Type Ii ◽  
Mucopolysaccharidosis Type Ii ◽  
The Central Nervous System

scholarly journals 369. AAV9 Mediated Correction of Iduronate-2-Sulfatase Deficiency in the Central Nervous System of Mucopolysaccharidosis Type II Mice

2015 ◽  
Vol 23 ◽  
pp. S146
Author(s):  
Kanut Laoharawee ◽  
Kelly M. Podetz-Pedersen ◽  
Kelley Kitto ◽  
Lucy Vulchanova ◽  
Carolyn Fairbanks ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mucopolysaccharidosis Type ◽  
Type Ii ◽  
Mucopolysaccharidosis Type Ii ◽  
The Central Nervous System
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