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 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A morphologic investigation of ependyma over gray matter (caudate nucleus) and over periventricular white matter (tapetum) of the rabbit lateral ventricle was undertaken prior to evaluation of morphological changes which occur with experimental hydrocephalus. Ependymal cells over the caudate nucleus are cuboidal and heavily ciliated. Numerous microvilli cover the cell surface. The lateral margins are straight and interdigitations between adjacent ependymal cells are absent. Ependymal cells over white matter are squamous. Nonciliated as well as ciliated cells contribute to the epithelial lining. Microvilli are present at the cell surface but tend to aggregate near the cellular borders. The lateral margins are convoluted and complex interdigitations are present between adjacent cells. Morphologic differences between ependymal cells over the caudate nucleus and those over periventricular white matter may help to explain the differential response to hydrocephalus observed in these two regions of the lateral ventricle.
Anat Rec 1979 May
PMID:The morphology of extrachoroidal ependyma overlying gray and white matter in the rabbit lateral ventricle. 44 64

Hydrops allantois was diagnosed in two Haflinger mares with severe abdominal distension. Both mares were seven months pregnant. Abortion was induced with two injections of prostaglandin six hours apart followed by further manual dilation of the cervix and administration of oxytocin the next day. There were 90 and 95 litres of fluid, respectively, in the allantoic cavities which resembled extracellular fluid with regard to concentrations of urea, creatinine, sodium, potassium, calcium, magnesium, phosphate and chloride, but not total protein. Both fetuses had severe brain abnormalities which were diagnosed as cerebellar and cerebral hypoplasia associated with bilateral hydrocephalus internus and hydranencephaly and cerebellar aplasia, respectively. Both mares were pregnant by the same stallion, but a clear hereditary link was not found.
Vet Rec 1988 Nov 12
PMID:Two related cases of cerebellar abnormality in equine fetuses associated with hydrops of fetal membranes. 320 93

A 4-month-old male infant with 22q distal trisomy and karyotype 46,XY,rec(22), dup q,inv(22)(q13q12)mat is reported. This and six previous similar instances are compared, and a distinct syndrome is delineated as follows: growth and psychomotor retardation, microcephaly or hydrocephaly, brain malformation, defective skull ossification, hypertelorism, narrow palpebral fissures, short broad nose, cleft palate with or without lip involvement, short neck, cardiac defect, renal and genital hypoplasia, osteoarticular abnormalities (mostly clubfoot), and poor survival. In addition, this syndrome is distinct from other duplications of chromosome 22, namely the complete trisomy, the proximal trisomy, and the cat-eye phenotype.
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PMID:The 22q distal trisomy syndrome in a recombinant child. 325 93

A family of bull mastiff pups in which 16 animals developed certain neurological signs is described. It is probable that the disease is inherited in an autosomal recessive manner. Clinical and pathological examination of six animals revealed ataxia, behavioural abnormalities and a visual defect associated with symmetrical lesions in the cerebellar nuclei, lateral vestibular nucleus and inferior colliculus together with a communicating hydrocephalus. The cerebellar lesions consisted of vacuolation, gliosis and axonal degeneration. Evidence for both axonal and oligodendroglial abnormalities was present and these probably result from a genetically determined metabolic disturbance in the affected neurones.
Vet Rec 1983 Apr 09
PMID:Familial cerebellar ataxia with hydrocephalus in bull mastiffs. 685 76

Neurological examination of a lethargic, ataxic 12-week-old dobermann revealed decreased conscious proprioception in all its limbs. Haematological examination revealed a low platelet count. Cytological examination of a sample of cerebrospinal fluid revealed evidence of haemorrhage and chronic inflammation. The levels of von Willebrand's factor antigen were extremely low. Skull radiographs were consistent with mild hydrocephalus. Treatment resulted in little clinical improvement and the animal was euthanased. Post mortem examination of the brain revealed an internal hydrocephalus with haemorrhage into the ventricles. It was considered that the animal had suffered severe intracranial haemorrhage as a result of its low level of von Willebrand's factor antigen and that the bleeding may have been potentiated by the low platelet count.
Vet Rec 1995 Jun 24
PMID:Intracranial haemorrhage in a dobermann puppy with von Willebrand's disease. 757 Dec 71

Cholesterinic granulomas have been previously reported as an incidental post mortem in horses. Three adult horses with diencephalic dysfunction due to cholesterinic granulomas are described. All the horses exhibited profound depression, somnolence and reluctance to move. One horse experienced generalised seizures. Cerebrosinal fluid was xanthochromic with an elevated total protein in two of the cases evaluated. The large cholesterinic granulomas caused expansion of the lateral ventricle and secondary hydrocephalus due to the build up of cerebrospinal fluid behind the mass. Cholesterinic granulomas are believed to result from choroid plexus congestion and haemorrhage.
Vet Rec 1994 Sep 03
PMID:Neurological manifestation of cholesterinic granulomas in three horses. 781 10

Stenosis of the cerebral aqueduct seems to be a key event for the development of congenital hydrocephalus. The causes of such a stenosis are not well known. Overholser et al. in 1954 (Anat Rec 120:917-933) proposed the hypothesis that a dysfunction of the subcommissural organ (SCO) leads to aqueductal stenosis and congenital hydrocephalus. The SCO is a brain gland, located at the entrance of the cerebral aqueduct, that secretes glycoproteins into the cerebrospinal fluid that, upon release, assemble into a fibrous structure known as Reissner's fiber (RF). By the permanent addition of new molecules to its rostral end, RF grows and extends along the aqueduct, fourth ventricle, and central canal of the spinal cord. The immunological blockage of the SCO-RF complex has been used to test Overholser's hypothesis. The following was the sequence of events occurring in pregnant rats that had been immunized with RF glycoproteins: the mother produced anti-RF antibodies and transferred them to the fetus through the placenta and to the pup through the milk, and the antibodies reached the brain of the fetus and pup and blocked the SCO-RF complex. This resulted in a permanent absence of RF that was followed by stenosis of the cerebral aqueduct, and then by the appearance of hydrocephalus. The latter was patent until the end of the 6-month observation period. The chronic hydrocephalic state appeared, in turn, to induce new alterations of the SCO. It is concluded that a selective immunological knock out of the SCO-RF complex leads to hydrocephalus.
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PMID:Hydrocephalus induced by immunological blockage of the subcommissural organ-Reissner's fiber (RF) complex by maternal transfer of anti-RF antibodies. 1110 26

In human beings a Chiari type 1 malformation is a developmental condition characterised by cerebellar herniation and syringohydromyelia. Abnormalities compatible with such a malformation were identified by magnetic resonance imaging in 39 cavalier King Charles spaniels with neurological signs and in one neurologically normal cavalier King Charles spaniel that was examined postmortem. The dogs with these abnormalities had a wide variety of neurological signs, but there was no apparent correlation between the neurological signs and the severity of cerebellar herniation, syringohydromyelia or hydrocephalus.
Vet Rec 2003 Aug 30
PMID:Neurological signs and results of magnetic resonance imaging in 40 cavalier King Charles spaniels with Chiari type 1-like malformations. 1297 37

Rodent models of polycystic kidney disease (PKD) have provided valuable insight into the cellular changes associated with cystogenesis in humans. The present study characterizes the morphology of renal and extrarenal pathology of autosomal recessive PKD induced by the wpk gene in Wistar rats. In wpk(-/-) rats, proximal tubule and collecting duct cysts develop in utero and eventually consume the kidney. Increased apoptosis, mitosis, and extracellular tenascin deposition parallel cyst development. Extrarenal pathology occurs in the immune system (thymic and splenic hypoplasia) and central nervous system (CNS; hypoplasia to agenesis of the corpus callosum with severe hydrocephalus). Severity of hydrocephalus varied inversely with size of the corpus callosum. In wpk(-/-) rats, the corpus callosum exhibits relatively few axons that cross the midline. This CNS pathology is similar to that described in three human renal cystic syndromes: orofaciodigital, genitopatellar, and cerebrorenal-digital syndromes. Collecting duct and ventricular ependymal cilia appear morphologically normal. To determine if rodent background strain and the presence of modifier genes affect severity of the disease, we crossed the Wistar-wpk rat with Brown Norway (BN) and Long Evan (LE) rats and found the degree of renal and cerebral pathology was diminished as evidenced by lower kidney weight as a percent of body weight and serum urea nitrogen concentration in cystic rats on LE or BN strains as well as less prominent cranial enlargement. Crosses with BN rats allowed us to localize the wpk gene on chromosome 5 very close to the D5Rat73 marker. The wpk gene lies within a chromosomal region known to harbor a PKD modifier locus. In summary, the types of renal and cerebral pathology seen in the Wistar wpk rat are a unique combination seen only in this rodent model.
Anat Rec A Discov Mol Cell Evol Biol 2004 Apr
PMID:Development of multiorgan pathology in the wpk rat model of polycystic kidney disease. 1505 65

A dog with hydrocephalus as a result of aqueduct stenosis and cerebellar herniation underwent ventriculoperitoneal shunting. Magnetic resonance images and computed tomography scans taken after the surgery revealed subdural accumulations of haemorrhagic fluid and cereberocortical collapse caused by overshunting and leakage of cerebrospinal fluid from the site of insertion of the shunt. However, the degree of cerebellar herniation was reduced after the shunt was inserted, and the dog did not develop any neurological signs and made good progress.
Vet Rec 2005 Feb 12
PMID:Subdural accumulation of fluid in a dog after the insertion of a ventriculoperitoneal shunt. 1574 57


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