Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nomenclature, life cycles, and pathogenicity of Sarcocystis of domestic animals are reviewed. Sarcocystis had a 2-host life cycle, with carnivores as definitive hosts and herbivores as intermediate hosts. The following species are found in domestic animals (with the definitive hosts given in parentheses): 3 species in the ox: S cruzi (dog, wolf, coyote, raccoon, fox), S hirsuta (cat), S hominis (man, monkey); 2 species in the sheep: S ovicanis (dog), S tenella (cat); 3 species in the pig: S miescheriana (dog), S porcifelis n sp (cat), S porcihominis n sp (man); and 1 species in the horse: S bertrami (dog). Sarcocystis cruzi, S ovicanis, and S porcifelis are highly pathogenic to the ox, the sheep, and the pig, respectively. Clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42 C, or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation, and loss of hair at the tip of the tail. Anemia, anorexia, ataxia, and abortions are the chief clinical signs of acute ovine sarcocystosis. These signs are evident at the time of vascular endothelium is parasitized by schizonts. The schizonts disappear in about 1 month, and cysts are formed in the muscles. The cystic phase of sarcocystosis is virtually nonpathogenic. Carnivores shed sporocysts in their feces after ingesting the intramuscular cysts from the herbivores. Sarcocystis is nonpathogenic to the definitive host. Feline and canine coccidia are also reviewed. The following 11 species are found in cats: Toxoplasma gondii, Hammondia hammondi, Isospora felis, Isosporarivolta, Besnoitia besnoiti, Besnoitia sp, and 5 types of Sarcocystis (S hirsuta from the ox, S tenella from the sheep, S muris from the mouse, S porcifelis from the pig, and Sarcocystis sp from Grant's gazelle). The following 10 species are found in canine feces (Isospora canis, Isospora ohioensis, Isospora wallacei n sp; and 7 types of Sarcocystis (S cruzi from the ox, S ovicanis from the sheep, S bertrami and Sarcocystis sp from the horse, S miescheriana from the pig, S hemionilatrantis from mule deer, and Sarcocystis sp from Grant's gazelle). The history of Isospora begemina in dogs is reviewed; life cycles of feline and canine coccidia are given; oocysts of common feline and canine coccidia are compared and illustrated; and public health significance of Toxoplasma gondii oocysts is discussed, especially in relation to cats in the household of pregnant women.
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PMID:A review of Sarcocystis of domestic animals and of other coccidia of cats and dogs. 82 60

Several birds in a flock of 40 Roller canaries (Serinus canaria) from an outdoor aviary in Victoria, Australia, developed central nervous system signs that included blindness, nystagmus, ataxia, and head rotation. Four died, and four were euthanatized. Two euthanatized birds were submitted for microscopic examination of tissues. Brain lesions in both birds consisted of scattered foci of nonsuppurative meningoencephalitis with gliosis, mild to moderately extensive lymphocytic/plasmacytic perivascular cuffs, and a patchy increased prominence of cerebral blood vessels associated with hypertrophy of the vascular endothelium and/or thickening of their connective tissue walls. These lesions were associated with the presence of Toxoplasma gondii tissue cysts. Lesions in the eyes of both birds were bilateral and consisted of severe plasmacytic/granulomatous ophthalmitis. Surviving birds were treated with trimethoprim and sulfadiazine, no subsequent deaths occurred, and no new cases developed over an 8-month period.
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PMID:Central nervous system toxoplasmosis in Roller canaries. 779 85

Blood-brain barrier (BBB) breakdown is a feature of cerebral ischaemia, multiple sclerosis, and other neurodegenerative diseases, yet the relationship between astrocytes and the BBB integrity remains unclear. We present a simple in vivo model in which primary astrocyte loss is followed by microvascular damage, using the metabolic toxin 3-chloropropanediol (S-alpha-chlorohydrin). This model is uncomplicated by trauma, ischaemia, or primary immune involvement, permitting the study of the role of astrocytes in vascular endothelium integrity, maintenance of the BBB, and neuronal function. Male Fisher F344 rats given 3-chloropropanediol show astrocytic damage and death at 4-24 h in symmetrical brainstem and midbrain nuclear lesions, while neurons show morphological changes at 24-48 h. Fluorescent 10 kDa dextran tracers show the BBB leaking from 24 h, progressing to petechial haemorrhage after 48-72 h, with apparent repair after 6 days. BBB breakdown, but not the earlier astrocytic death, is accompanied by a delayed increase in blood flow in the inferior colliculus. An ED1 inflammatory response develops well after astrocyte loss, suggesting that inflammation may not be a factor in starting BBB breakdown. This model demonstrates that the BBB can self-repair despite the apparent absence of direct astrocytic-endothelial contact. The temporal separation of pathological events allows pharmacological intervention, and the mild reversible ataxia permits long-term survival studies of repair mechanisms.
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PMID:Focal astrocyte loss is followed by microvascular damage, with subsequent repair of the blood-brain barrier in the apparent absence of direct astrocytic contact. 1496 64

Mouse embryos genetically null for all alphav integrins develop intracerebral hemorrhage owing to defective interactions between blood vessels and brain parenchymal cells. Here, we have used conditional knockout technology to address whether the cerebral hemorrhage is due to primary defects in vascular or neural cell types. We show that ablating alphav expression in the vascular endothelium has no detectable effect on cerebral blood vessel development, whereas deletion of alphav expression in central nervous system glial cells leads to embryonic and neonatal cerebral hemorrhage. Conditional deletion of alphav integrin in both central nervous system glia and neurons also leads to cerebral hemorrhage, but additionally to severe neurological defects. Approximately 30% of these mutants develop seizures and die by 4 weeks of age. The remaining mutants survive for several months, but develop axonal deterioration in the spinal cord and cerebellum, leading to ataxia and loss of hindlimb coordination. Collectively, these data provide evidence that alphav integrins on embryonic central nervous system neural cells, particularly glia, are necessary for proper cerebral blood vessel development, and also reveal a novel function for alphav integrins expressed on axons in the postnatal central nervous system.
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PMID:Selective ablation of alphav integrins in the central nervous system leads to cerebral hemorrhage, seizures, axonal degeneration and premature death. 1557 10

Nine weaned Labrador Retriever puppies from a litter of 11 were presented with signs of acute central nervous system (CNS) disease that included ataxia and blindness. All puppies died. Gross examination of tissues from 2 puppies revealed regionally diffuse hemorrhages in the brain stem and swollen hemorrhagic lymph nodes. Light microscopic examination of hematoxylin and eosin-stained tissues showed numerous large, basophilic intranuclear inclusion bodies within CNS vascular endothelium and occasionally in individual hepatocytes. Immunohistochemical staining of the tissue was positive using an antibody against canine adenovirus-1. Virus isolation for infectious canine hepatitis virus was achieved using inoculated cell cultures. Polymerase chain reaction amplification of DNA from cell culture material revealed shared homology with other mammalian adenoviruses.
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PMID:Diagnosis of infectious canine hepatitis virus (CAV-1) infection in puppies with encephalopathy. 1569 Sep 52

Calcium-activated potassium channels modulate calcium signaling cascades and membrane potential in both excitable and non-excitable cells. In this article we will review the physiological properties, the structure activity relationships of the existing peptide and small molecule modulators and the therapeutic importance of the three small-conductance channels KCa2.1-KCa2.3 (a.k.a. SK1-SK3) and the intermediate-conductance channel KCa3.1 (a.k.a. IKCa1). The apamin-sensitive KCa2 channels contribute to the medium afterhyperpolarization and are crucial regulators of neuronal excitability. Based on behavioral studies with apamin and on observations made in several transgenic mouse models, KCa2 channels have been proposed as targets for the treatment of ataxia, epilepsy, memory disorders and possibly schizophrenia and Parkinson's disease. In contrast, KCa3.1 channels are found in lymphocytes, erythrocytes, fibroblasts, proliferating vascular smooth muscle cells, vascular endothelium and intestinal and airway epithelia and are therefore regarded as targets for various diseases involving these tissues. Since two classes of potent and selective small molecule KCa3.1 blocker, triarylmethanes and cyclohexadienes, have been identified, several of these postulates have already been validated in animal models. The triarylmethane ICA-17043 is currently in phase III clinical trials for sickle cell anemia while another triarylmethane, TRAM-34, has been shown to prevent vascular restenosis in rats and experimental autoimmune encephalomyelitis in mice. Experiments showing that a cyclohexadiene KCa3.1 blocker reduces infarct volume in a rat subdural hematoma model further suggest KCa3.1 as a target for the treatment of traumatic and possibly ischemic brain injury. Taken together KCa2 and KCa3.1 channels constitute attractive new targets for several diseases that currently have no effective therapies.
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PMID:Modulators of small- and intermediate-conductance calcium-activated potassium channels and their therapeutic indications. 1758 55