Gene/Protein Disease Symptom Drug Enzyme Compound
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 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper presents data from the literature and the author's own materials on the correlation between the extent of activity of reparation processes and the development of cell malignization. A review cites the results of investigations on the molecular mechanisms in some hereditary human diseases in which a defect in some stages of the reparation processes has been found (xeroderma, ataxia telangesthesia. Fanconi anemia, Down's syndrome, etc.). These diseases are also characterized by a high rate of neoplasia development. It is emphasized that inhibition of the reparation process is observed only in the first stages of normal cell transformation into a malignant one. A correlation between carcinogenic and mutagenic activity of chemical compounds which is in favour of the mutation hypothesis of the origin of tumours is discussed.
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PMID:[Mechanisms of carcinogenesis associated with DNA repair]. 15 41

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31

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

An epileptic patient on chronic anticonvulsant drug therapy is described, in whom anaemia and neurological abnormalities including progressive dementia, bilateral pyramidal tract signs, incontinence and ataxia developed. Vitamin B12 serum levels and absorption were normal, but serum folic acid levels were low. Both the neurological disturbances and anaemia resolved following oral folic acid administration. This sequence of events in our patient suggests a cause and effect relationship between the folate deficiency and the coexistent, transient neurological syndrome.
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PMID:Reversible central nervous system dysfunction in folate deficiency. 114 59

A 48-year-old man, who took by mistake a sip of ointment containing dichloroethane, survived, and showed a course of two phases of toxic symptoms. After an initial narcosis and an interval with few pathological symptoms seizures, myoclonia and somnolence occurred. Irreversible final disturbances were lasting mental defects, cerebellar dysarthria, ataxia, and hydrocephalus. Concomitant diseases were acute liver dystrophy, nephropathy, and anemia. The clinical picture of dichoroethane posoning is outlines, the pathogenesis of this particular cerebral lesion described, and the therapy discussed.
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PMID:[Dichloroethane poisoning with myoclonic syndrome, seizures and irreversible cerebral defects (author's transl)]. 122 Jun 46

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Clostridium septicum infection causing 5.0 to 5.2% mortality is reported for the first time in the literature from six-week-old growing geese in three flocks comprising 5,200, 5,500 and 5,900 geese, respectively. The affected birds exhibited weakness, uncoordinated movement, ataxia and, frequently, oblique position of the head and neck (torticollis) as well as signs indicative of dysequilibrium. The affected birds died within 18-24 h. Gross pathological examination revealed anaemia, hepatitis with map-like necroses of irregular outline (Fig. 1), acute enteritis, pulmonary oedema and cardiac dilatation. Light and electron-microscopic examination showed that the sinusoids of the liver were markedly dilated (Fig. 2) and filled with serous exudate and gas (Figs 2 and 3), and the hepatocytes surrounding them exhibited severe oedema (Fig. 4). Among the hepatocytes, ciliated bacteria 7-10 mu in length and 1-3 mu in width, bounded by a well-defined cell wall and often showing signs of spore formation were observed (Figs 5 and 6). By bacteriological examination the pathogen was isolated, its properties were studied, and the clinical entity of malignant oedema was experimentally reproduced by intramuscular injection of guinea-pigs and rabbits. The applied antibiotic (oxytetracycline) and furazolidone therapy proved effective.
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PMID:Demonstration of Clostridium septicum infection in a goose flock. 147 92

A patient with hepatitis B virus-associated cirrhosis manifested various symptoms such as anemia, renal damage and neurological signs including cerebellar ataxia due to long-term administration of germanium-containing food. The patient was a 40-year-old male who had taken germanium containing mineral cheese for 26 months after he was diagnosed as having cirrhosis. Twenty four months after beginning to take the mineral cheese, he began manifesting paresthesia of the extremities, dysarthria and gait ataxia. Laboratory findings revealed anemia and renal damage. Biopsy of the peripheral nerve revealed loss of the large sheathed nerve, a characteristic feature of germanium intoxication. A high concentration of germanium (GeO2) was detected in patient's hair and urine. Cerebellar ataxia was characteristic in this patient, which was not reported in the previous papers.
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PMID:[A patient with liver cirrhosis manifesting various symptoms including cerebellar ataxia due to germanium intoxication]. 155 52

Clinical characteristics were examined in 5 elderly patients whose brain showed typical features of Wernicke's encephalopathy at the autopsy. All 5 were females with a mean age of 67 +/- 4 years old. The pathological diagnosis of Wernicke's encephalopathy was based on the presence of bleeding or atrophy of bilateral mammilary bodies, proliferation of capillaries and increase of macrophages in mammilary bodies, midbrain periaqueductal gray matter and periventricular area, with relatively intact neurons. Wernicke's encephalopathy was diagnosed clinically only in one case. The remaining four had no clinical diagnosis of Wernicke's encephalopathy. Underlying diseases were varied including neurological, metabolic, gastrointestinal disorders and malignancy. The predominant symptom, consciousness disturbance, was seen in 4 cases. Two of them showed a comatose state. Ocular symptoms and ataxia were observed in 2 cases. Laboratory findings revealed leukocytosis and anemia in 3 cases, hypoproteinemia in 4 cases. One case was alcoholic, but the other four were non-alcoholics and developed the disease after prolonged malnutrition. At the onset of the disease, 4 cases were receiving glucose and electrolyte infusion without vitamins, at the onset of the disease. We propose that in elderly patients with consciousness disturbance of unknown cause, Wernicke's encephalopathy should be taken into consideration even in non-alcoholics, and thiamine infusion should be commenced at once when the disease is suspected even when typical symptoms are lacking.
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PMID:[Clinical characteristics of Wernicke's encephalopathy in the elderly]. 156 Jun 7

We report here an autopsy case of chronic germanium intoxication with major pathological changes in the central and peripheral sensory nervous systems. The patient was a 4-year-old girl who had suffered from gait disturbance and generalized muscle weakness for 22 months. She had been given orally germanium compounds (containing germanium dioxide, 225-450 mg/day) for the previous 28 months. In addition to the findings of chronic renal failure and anemia, she presented characteristic neurological symptoms exemplified by diffuse muscle atrophy, tongue fasciculation, sensory impairment and truncal ataxia as well as areflexia. Median and ulnar sensory nerve conduction velocities were also reduced. On the 17th hospital day, she died of renal failure. In addition to conspicuous degeneration of renal tubular cells, pathological studies revealed marked nerve fiber loss, degeneration and gliosis in the dorsal column of the spinal cord, which were most conspicuous in the thoracic and cervical cord. Axonal degenerative changes were also conspicuous in the sural and sciatic nerves. High concentration of germanium was detected in the brain, cerebellum, spinal cord, sciatic nerve, liver and kidney. It was suggested that the neural involvement in the current case was caused by chronic toxicity of germanium.
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PMID:[An autopsy case of chronic germanium intoxication presenting peripheral neuropathy, spinal ataxia, and chronic renal failure]. 164 14


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