Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The technical grade of xylenes (mixed) (hereafter termed xylenes) contains the three isomeric forms and ethylbenzene (percentage composition shown above). The annual production for 1985 was approximately 7.4 x 108 gallons. Xylenes is used as a solvent and a cleaning agent and as a degreaser and is a constituent of aviation and automobile fuels. Xylenes is also used in the production of benzoic acid, phthalate anhydride, and isophthalic and terephthalic acids as well as their dimethyl esters. Toxicology and carcinogenesis studies of xylenes were conducted in laboratory animals because a large number of workers are exposed and because the long- term effects of exposure to xylenes were not known. Exposure for the present studies was by gavage in corn oil. In single-administration studies, groups of five F344/N rats and B6C3F1 mice of each sex received 500, 1,000, 2,000, 4,000, or 6,000 mg/kg. Administration of xylenes caused deaths at 6,000 mg/kg in rats and mice of each sex and at 4,000 mg/kg in male rats. In rats, clinical signs observed within 24 hours of dosing at 4,000 mg/kg included prostration, muscular incoordination, and loss of hind limb movement; these effects continued through the second week of observation. Tremors, prone position, and slowed breathing were recorded for mice on day 3, but all mice appeared normal by the end of the 2- week observation period. In 14- day studies, groups of five rats of each sex were administered 0, 125, 250, 500, 1,000, or 2,000 mg/kg, and groups of five mice of each sex received 0, 250, 500, 1,000, 2,000, or 4,000 mg/kg. Chemical- related mortality occurred only at 2,000 mg/kg in rats and at 4,000 mg/kg in mice. Rats and mice exhibited shallow breathing and prostration within 48 hours following dosing at 2,000 mg/kg. These signs persisted until day 12 for rats, but no clinical signs were noted during the second week for mice. In 13- week studies, groups of 10 rats of each sex received 0, 62.5, 125, 250, 500, or 1,000 mg/kg, and groups of 10 mice of each sex received 0, 125, 250, 500, 1,000, or 2,000 mg/kg. No deaths or clinical signs of toxicity were recorded in rats. However, high dose male rats gained 15% less weight and females 8% less weight than did the vehicle controls. Two female mice died at the 2,000 mg/kg dose. Lethargy, short and shallow breathing, unsteadiness, tremors, and paresis were observed for both sexes in the 2,000 mg/kg group within 5- 10 minutes after dosing and lasted for 15- 60 minutes. Two- year toxicology and carcinogenesis studies were conducted by administering 0, 250, or 500 mg/kg xylenes in corn oil by gavage to groups of 50 F344/N rats of each sex, 5 days per week for 103 weeks. Groups of 50 B6C3F1 mice of each sex were administered 0, 500, or 1,000 mg/kg xylenes on the same schedule. Although the mortality was dose related in male rats (final survival: vehicle control, 36/50; low dose, 26/50; high dose, 20/50), many of the early deaths in the dosed males were gavage related. Body weights of the high dose male rats were 5%- 8% lower than those of the vehicle controls after week 59. The mean body weights of low dose and vehicle control male rats and those of dosed and vehicle control female rats were comparable. Survival rates of female rats and both sexes of dosed mice were not significantly different from those of the vehicle controls. The mean weights of dosed male and female mice were comparable to those of the vehicle controls. Hyperactivity lasting 5- 30 minutes was observed in high dose mice after dosing, beginning after week 4 and continuing through week 103. At no site was the incidence of nonneoplastic or neoplastic lesions in dosed rats or mice of either sex considered to be related to the administration of xylenes. Neither xylenes nor any of its components (o- xylene, m-xylene, p- xylene, or ethylbenzene) were mutagenic when tested with or without metabolic activation in Salmonella typhimurium strains TA100, TA1535, TA97, or TA98 with the preincubation protocol. In addition, ethylbenzene was tested in cytogenetic assays using cultured Cetic assays using cultured Chinese hamster ovary cells both with and without metabolic activation; neither sister- chromatid exchanges nor chromosomal aberrations were induced by ethylbenzene. An audit of the experimental data was conducted for the 2-year studies of xylenes. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenicity of xylenes (mixed) for male or female F344/N rats given 250 or 500 mg/kg or for male or female B6C3F1 mice given 500 or 1,000 mg/kg.
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PMID:NTP Toxicology and Carcinogenesis Studies of Xylenes (Mixed) (60% m-Xylene, 14% p-Xylene, 9% o-Xylene, and 17% Ethylbenzene) (CAS No. 1330-20-7) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1273 97

Blastomycosis was diagnosed in six nondomestic felids from eastern Tennessee, including two Asian lions (Panthera leo persicus), one African lion (Panthera leo), one Siberian tiger (Panthera tigris), one cheetah (Acinonyx jubatus), and one snow leopard (Panthera uncia). Clinical signs included lethargy, anorexia, weight loss, dyspnea, sneezing. ataxia, and paresis. Variable nonspecific changes included leukocytosis, monocytosis, moderate left shift of neutrophils, moderate hypercalcemia, hyperproteinemia, and hyperglobulinemia. Thoracic radiographs revealed interstitial and alveolar changes, consolidation or collapse of a lung lobe, bullae formation, and a pulmonary mass. Agar gel immunodiffusion (AGID) serology for Blastomyces dermatitidis was performed in five felids and was positive in three. The tiger had cerebral blastomycosis and was positive for AGID serologic tests of both cerebrospinal fluid and serum. One percutaneous lung aspirate in the snow leopard and one bronchial aspirate in an Asian lion demonstrated B. dermatitidis organisms. whereas tracheal wash samples and a nasal discharge were nondiagnostic in others. Treatment with itraconazole was attempted in four cats. The tiger improved before euthanasia, whereas the others did not survive beyond initial treatments. In four felids, B. dermatitidis was found in the lungs and tracheobronchial lymph nodes associated with a florid pyogranulomatous reaction; the tiger had a pyogranulomatous encephalomyelitis, and the cheetah had a single pulmonary granuloma. Thoracic radiography, cytologic examination of lung lesion aspirates, and B. dermatitidis AGID serology should be performed on clinically ill zoo felids in endemic areas to rule out blastomycosis.
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PMID:Blastomycosis in nondomestic felids. 1458 83

Atherosclerosis is a common disease in parrots. The disease is found in all common parrot species, but especially in African Grey parrots and Amazons. It is a disease of older birds that is seen in both males and females. The most common sign is sudden death, but clinical symptoms that can be found include dyspnea, lethargy and nervous signs, such as paresis and collapses. Because the clinical signs are seldomly seen, it is difficult to diagnose atherosclerosis and therefore it is mostly an unexpected finding at necropsy. Age and species are determinants of atherosclerosis in parrots. Suggested risk factors include an elevated plasma cholesterol level, diet composition, social stress and inactivity, but research is needed to confirm this.
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PMID:Atherosclerosis in parrots. A review. 1523 50

A 63-year-old male presented with sudden onset of right hemiplegia and global aphasia. On admission he was stuporous. Computed tomography (CT) revealed no abnormalities except for right intraventricular meningioma found incidentally. Emergency angiography confirmed complete occlusion of the left internal carotid artery (ICA) and left M1 trunk whereas the left ICA bifurcation remained patent. The ipsilateral ICA was permanently occluded with two detachable balloons to prevent thrombus migration into the distal ICA and middle cerebral artery (MCA), followed by thrombolysis of the clot in the ipsilateral M1 through the contralateral ICA with urokinase (total dose 420,000 U) under systemic heparinization. Partial recanalization of the ipsilateral MCA was accomplished. The time interval from onset to recanalization was about 3 hours. Postoperative CT showed no hemorrhagic transformation. Slight right paresis and mild motor aphasia persisted 2 months later and he was transferred to a rehabilitation facility. Thrombolysis of the MCA embolism can be performed through the contralateral ICA in the presence of ipsilateral ICA occlusion.
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PMID:Middle cerebral artery thrombolysis through the contralateral internal carotid artery--case report. 1534 15

Ten dogs with neuroendocrine carcinoma of the liver were selected for inclusion in the study. Clinical signs were anorexia (7), vomiting (5), polydipsia/polyuria (3), icterus (2), lethargy (2), weight loss (2), paresis (1), ataxia (1), weakness (1), collapse (1), and urinary tract infection (1). Hematologic and biochemical abnormalities included anemia (2/8), leukocytosis (4/8), high liver enzyme activity (serum alkaline phosphatase, 7/9; alanine transaminase, 7/9; aspartate transaminase, 8/9), and high total bilirubin (6/9). Grossly, the tumors were diffuse, involving all liver lobes in six dogs, and two dogs had various-sized nodules in addition to diffuse involvement. Histologically, there were eight tumors with solid or trabecular pattern (group A), one tumor with cords or rows of neoplastic cells (group B), and one tumor with multiple rosette-like structures (group C). Immunohistochemical studies revealed that all 10 neoplasms were positive for at least one of the endocrine markers used: neuron-specific enolase (NSE; 8/10), synaptophysin (5/10), and chromogranin-A (3/10). A panel of NSE, chromagranin-A, and synaptophysin detected 100% of the tumors in our series. Electron microscopy confirmed the diagnosis by the presence of intracytoplasmic neurosecretory granules in the two examined cases. Our results show that neuroendocrine markers commonly used in humans can be used for the diagnosis of hepatic neuroendocrine carcinoma in dogs, preferably a panel of synaptophysin, chromagranin-A, and NSE because chromogranin-A alone is not as useful in dogs as in humans.
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PMID:Canine hepatic neuroendocrine carcinoma: an immunohistochemical and electron microscopic study. 1575 67

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with hyponatremia or its rapid correction, and chronic alcoholism is also a common underlying condition. We observed a 43-year-old man with diabetes mellitus who developed central pontine and extrapontine myelinolysis with no apparent evidence of hyponatremia, serum hyperosmolality or associated rapid correction, or history of alcohol abuse. On admission, the patient was lethargic with dysarthria, dysphagia, and mild tetraparesis and his face and lower extremities were severely edematous. Laboratory examination showed normoglycemia and normonatremia, although hypokalemia, elevated HbA1c, and nephrotic syndrome were also present. Magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pons, the deep layers of the cerebral cortex, and the adjacent white matter consistent with central pontine and extrapontine myelinolysis. Generalized edema was reduced by the use of diuretics and extracorporeal ultrafiltration without significant changes of serum sodium or osmolality. His consciousness level and paresis gradually improved within a few weeks. Our patient is a rare case of CPM associated with diabetes without apparent evidence of sodium or glucose imbalances.
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PMID:Central pontine and extrapontine myelinolysis associated with type 2 diabetic patient with hypokalemia. 1581 68

Here, we report the case of a five-year-old boy with carbonic monoxide (CO) poisoning. The patient initially recovered after the initiation of hyperbaric oxygen (HBO) therapy, but lethargy as well as visual and gait disturbances appeared two days later. Left hemiparesis and mood lability also subsequently appeared. Slow frontal activity was noted on electroencephalography, while fluid-attenuation inversion recovery and diffusion-weighted magnetic resonance imaging (MRI) revealed high signal-intensity lesions in the hippocampus and deeper layers of the occipital and frontal cerebral cortex. The neurological symptoms subsided gradually during the 10-day course of HBO therapy, but the left-hand paresis and quadrantic hemianopsia persisted, in association with impaired attention, slow mental processing, and incontinence. Lesions in the globus pallidum were noted on follow-up MRI at 14 days, and cortical lesions became evident as linear, low signal-intensity areas on T1-weighted imaging 4 months after presentation. Delayed neuropsychiatric syndrome in CO poisoning is rare in childhood, although children should be carefully monitored after CO exposure. The finding of cortical laminar necrosis in this patient is quite atypical in CO poisoning, and suggests a broader and previously nonpredicted pathomechanism in this condition.
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PMID:Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning. 1700 41

The incidence of intracranial aneurysms in infancy is relatively rare. They are infrequent in children less than 1 year old, and are an exception in the neonatal period. They usually originate in the internal carotid artery bifurcation, posterior circulation and seldom in the territory of the distal middle cerebral artery distribution. Infants often present with nonspecific symptoms: irritability, lethargy, vomiting, seizures and coma. Sometimes, they may present with unexpected clinical symptoms such as peripheral facial palsy. Subarachnoid hemorrhage is the most frequent presentation in this kind of aneurysms. Intracerebral hematoma is unusual. We present the case of a 10-week-old child harboring a middle cerebral artery aneurysm. To our knowledge, this is the first case of an aneurysm presenting as a peripheral facial paresis in a pediatric patient.
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PMID:Congenital aneurysm presenting as peripheral facial paresis. 1799 41

Alphaviruses (Togaviridae) infect wild birds, but clinical illness and death attributable to virus in naturally infected birds is rarely reported, particularly for small passerine species or nestlings. Buggy Creek virus is a unique alphavirus in the Western equine encephalomyelitis virus (WEEV) complex that is vectored by the cimicid swallow bug (Oeciacus vicarius), an ectoparasite of the colonially nesting Cliff Swallow (Petrochelidon pyrrhonota) and the introduced House Sparrow (Passer domesticus). While sampling birds for Buggy Creek virus (BCRV) during the summers of 2007 and 2008, we discovered large numbers of clinically ill or dead House Sparrow nestlings. Ill nestlings exhibited ataxia, torticollis, paresis, and lethargy. Histologic examination revealed that encephalitis was the most common finding, followed by myositis, myocarditis, and hepatic changes, but pathology was highly variable. We isolated BCRV from brain tissue in most of the ill or dead nestlings, and from blood, liver, kidney, spleen, lung, feather pulp, and skin in some birds. To our knowledge, this is the first report of clinical illness, gross pathology, and histopathology for a WEEV-complex alphavirus in a field-collected passerine species.
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PMID:Pathology and virus detection in tissues of nestling house sparrows naturally infected with Buggy Creek virus (Togaviridae). 2009 15

A 16-yr-old female blue and gold macaw (Ara ararauna) was presented with an acute history of lethargy, inappetance, ataxia, and paralysis. The bird had rapidly progressed from a normal state to complete inability to perch or ambulate within a 48-hr period. Neurologic examination revealed bilateral hind limb paresis with upper motor neuron signs present in both legs and the vent. Radiographs identified multiple nodular soft-tissue opacities within the cranial coelomic cavity and a single nodule superimposed with the thoracic spine. The bird was euthanized and submitted for necropsy, which revealed a primary pulmonary adenocarcinoma with multiple sites of osseous metastasis, including the vertebrae, and subsequent spinal cord compression. This is the first report of pulmonary adenocarcinoma in this species, although reports of similar tumors in other psittacines have been published. This report, along with others previously published, suggests that vertebral metastasis of primary pulmonary tumors may be more common in psittacine species than previously recognized and, as such, should be considered as a differential diagnosis in psittacine birds exhibiting signs of neurologic dysfunction attributed to a spinal cord lesion.
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PMID:Pulmonary adenocarcinoma with osseous metastasis and secondary paresis in a blue and gold macaw (Ara ararauna). 2327 61


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