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hydrocephalus/l tyrosine
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Gain-of-function mutations in the gene encoding the tyrosine phosphatase SHP2 induce hydrocephalus in a catalytically dependent manner.
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Catalytically activating mutations in Ptpn11, which encodes the protein tyrosine phosphatase SHP2, cause 50% of Noonan syndrome (NS) cases, whereas inactivating mutations in Ptpn11 are responsible for nearly all cases of the similar, but distinct, developmental disorder Noonan syndrome with multiple
Loss of Fyn tyrosine kinase on the C57BL/6 genetic background causes hydrocephalus with defects in oligodendrocyte development.
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The supportive functions of oligodendrocytes are required for the survival and development of axons, ensuring the organization of highly specialized neuronal networks in brain. Although the molecules that regulate oligodendrocyte differentiation in vitro have been identified, their roles in vivo are
Anxiety responses and neurochemical changes in a kaolin-induced rat model of hydrocephalus.
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OBJECTIVE
Hydrocephalus is a pathological enlargement of the ventricles of the brain, which can result from various diseases of the central nervous system. Patients with hydrocephalus frequently show motor abnormalities, such as abnormal gait and posture, as well as intellectual and emotional
Reversibility of functionally injured neurotransmitter systems with shunt placement in hydrocephalic rats: implications for intellectual impairment in hydrocephalus.
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Intellectual impairment has been related to alteration of neuronal innervation in the following regions: cholinergic basal forebrain nuclei (Ch1-Ch6, learning and memory), dopaminergic ventral tegmental area (emotional control), and noradrenergic locus ceruleus (cognition). Recent studies have
Novel missense mutation in the L1 gene in a child with corpus callosum agenesis, retardation, adducted thumbs, spastic paraparesis, and hydrocephalus.
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Corpus callosum agenesis, retardation, adducted thumbs, spastic paraparesis, and hydrocephalus (CRASH syndrome) is an X-linked recessive disorder caused by mutations in the neuronal cell adhesion molecule L1 (LICAM) gene. L1 plays a key role in axon outgrowth and pathfinding during the development
The behavioral change of locomotor activity in a kaolin-induced hydrocephalus rat model: evaluation of the effect on the dopaminergic system with progressive ventricle dilatation.
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Hydrocephalus is a pathological enlargement of the cerebral ventricle that results from an obstruction of the space containing cerebrospinal fluid (CSF) in the brain. Motor abnormalities, such as abnormal gait and posture, are frequently seen in patients with hydrocephalus. The present study was
[Pathology of congenital aqueductal stenosis and posthemorrhagic hydrocephalus].
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The brain stem of children with congenital aqueductal stenosis or posthemorrhagic hydrocephalus were examined histologically and immunohistochemically. Congenital aqueductal stenosis occurs in various stages of CNS development, and is associated with microdysplasia and maturational abnormalities
Periaqueductal microdysplasia in children with congenital aqueductal stenosis.
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The brainstems of children with aqueductal stenosis (AS) and controls were examined histologically and immunohistochemically. In the periaqueductal area of children with AS, there was astrogliosis, loss of neurons (tyrosine-hydroxylase (TH) reactivity) and decreased myelination (myelin basic protein
Neuropathology and immunohistochemistry of the brain-stem in neonates with congenital hydrocephalus: comparative studies between aqueductal stenosis and Arnold-Chiari malformation.
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Neuropathological and immunohistochemical studies were done on the brain-stem of neonates who had congenital hydrocephalus with aqueductal stenosis or Arnold-Chiari malformation (ACM). The infants with aqueductal stenosis showed heterogeneity in their clinicopathological findings while the infants
Functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia of adult rat with kaolin-induced hydrocephalus.
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Structural and/or functional injury of the basal ganglia can lead to motor functional disabilities, abnormal gait and posture, and intellectual/emotional impairment, disorders also frequently seen in hydrocephalus. Previous reports have documented changes in dopamine levels in the neostriatum in
Use of a novel double-sandwich enzyme-linked immunosorbent assay method for assaying chondroitin sulfate proteoglycans that bear 3-nitrotyrosine core protein modifications, a previously unrecognized proteoglycan modification in hydrocephalus.
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3-Nitrotyrosine is a useful marker for nitric oxide-mediated tissue injury. However, which proteins are preferred peroxynitrite modification targets is unclear. Chondroitin sulfate proteoglycans (CSPGs) abnormally accumulate in cerebrospinal fluid of human neonates with hydrocephalus and may be a
Catecholamine alterations in experimental hydrocephalus.
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Experimental hydrocephalus was induced in rats by intracisternal injection of kaolin suspension. The amounts of norepinephrine and dopamine were determined in the whole brain and specific brain regions at 1 week (acute phase) and 4 weeks (chronic phase). The turnover of catecholamine, an index of
Tubulin tyrosine ligase-like 1 deficiency results in chronic rhinosinusitis and abnormal development of spermatid flagella in mice.
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Tubulin tyrosine ligase-like 1 (TTLL1) protein is a member of the tubulin tyrosine ligase superfamily of proteins that are involved in the posttranslational polyglutamylation of tubulin in axonemal microtubules within cilia and flagella. To investigate the physiological role of TTLL1, the authors
PTPRQ as a potential biomarker for idiopathic normal pressure hydrocephalus.
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Idiopathic normal pressure hydrocephalus (iNPH) is caused by the accumulation of cerebrospinal fluid (CSF) and is characterized by gait disturbance, urinary incontinence, and dementia. iNPH dementia is treatable by shunt operation; however, since the cognitive symptoms of iNPH are often similar to
Palliative cerebrospinal fluid shunting for leptomeningeal metastasis-related hydrocephalus in patients with lung adenocarcinoma: A single-center retrospective study.
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