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Male rats were treated with phenobarbital, a dinitrotoluene (2,4-DNT or 2,6-DNT), or 2,4,6-trinitrotoluene (2,4,6-TNT); and the biotransformation of model xenobiotics was determined. Phenobarbital produced a stimulation, and 2,6-DNT produced a biphasic effect in biotransformation.
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Experimental infection of golden hamsters with the hookworm, Ancylostoma ceylanicum, caused a profound decline in the hepatic microsomal cytochrome P450 content. Concomitant decrease was also noticed in aminopyrine N-demethylase and benzo[a]pyrene hydroxylase activities. However, aniline hydroxylase activity was only marginally elevated during the infection. Microsomal markers, viz., cytochrome b5, NADH-cytochrome-c reductase, and glucose-6-phosphatase, were not significantly altered. Hepatic tissue exhibited an accumulation of lipids, especially phospholipids, triglycerides, and cholesterol, resulting in fatty necrosis around the central vein region. Isolated hepatic microsomes showed a decrease in phosphatidylcholine content. Impairment in hepatic mixed function oxidase (MFO) activities was further confirmed by prolongation in hexobarbital sleeping time and zoxazolamine-induced paralysis. The hepatic MFO system of A. ceylanicum-infected hamsters responded qualitatively and quantitatively in a manner similar to that of control hamsters, upon stimulation with selective chemical inducers like phenobarbitone and 3-methylcholanthrene. Kinetic and in vitro substrate binding studies revealed that for aminopyrine the substrate affinity and the maximum enzyme activity (Vmax) were decreased, while for aniline the binding affinity was decreased and the binding capacity was enhanced. Results indicate specific/selective impairment of the hepatic microsomal cytochrome P450 system during hookworm infection and may have many practical implications in toxicology and pharmacology.
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PURPOSE: The purpose of this study was to review the incidence and clinical presentation of vertebral metastases related to squamous cell carcinoma of the oral cavity. PATIENTS AND METHODS: We conducted a retrospective review of our clinical experience with 597 cases of squamous cell carcinoma of the oral cavity. RESULTS: Four patients with vertebral metastases were identified, accounting for 0.7% of the series. Thirteen vertebrae were involved in these 4 patients. All patients showed advanced cervical metastases as evidenced by several histologically positive nodes with extracapsular invasion when the ablative tumor specimen was examined. All patients displayed symptoms of their vertebral metastases, including severe pain, hypercalcemic somnolence, and flaccid paralysis of the lower extremities as part of the cauda equina syndrome. CONCLUSIONS: Vertebral metastases are rare forms of distant metastasis related to squamous cell carcinoma of the oral cavity. Bone pain is a symptom that should result in expedient radiographic examination in such patients, particularly when advanced cervical metastases are identified during the primary tumor surgery, which places the patient at risk for distant metastatic disease.
Electromyography and conduction studies in motor and sensory fibres were performed in 58 patients with different types of radial nerve injury. The site of nerve injury was predicted by clinical and electromyographic findings and correlated with changes in conduction, thereby permitting a more exact classification of the type of nerve injury. In patients with Saturday-night palsy, there was considerable slowing of conduction in both motor and sensory fibres across the presumed site of the lesion with return to normality within six to eight weeks. These observations suggest that local demyelination is the cause of nerve palsy. There were changes in sensory conduction even when there was no sensory deficit clinically, with no difference in susceptibility of motor and sensory fibres to ischaemia. In patients with radial nerve palsy secondary to fracture of the humerus, out-growth in motor and sensory fibres was equal and estimated to be about 1 mm per day. When the radial nerve palsy was attributed to traction or mild blunt injury the site of lesion was based on clinical and electromyographic findings. The rate of conduction in motor and sensory fibres was normal, suggesting that axonal damage was the cause of paresis, with sparing of some of the fastest conducting fibres.
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The activities of some hepatic microsomal drug metabolizing enzymes, which are markedly depressed in mice infected with Schistosoma mansoni, can be increased by treatment with phenobarbital or 3-methylcholanthrene. Administration of these compounds to infected mice increased the capacity of the liver to metabolize drugs up to the maximum level inducible in non-infected animals. However, the increased hepatic microsomal mass, reflected in glucose 6-phosphatase activities and cytochrome b5 levels, observed in schistosome-infected mice, was not increased further by the same treatment. The changes in the activities of several drug metabolizing enzymes in vitro were confirmed in vivo by determination of hexobarbital-induced sleeping time and zoxazolamine-induced paralysis duration.
Progressive supranuclear palsy, first described as clinical entity by Steele, Richardson and Olszewski, is a degenerative disorder of the central nervous system. Besides progressive supranuclear oculomotor disturbances, other characteristic signs are pseudobulbar paresis, axial rigidity, gait disturbances and subcortical dementia. Misinterpretation in the early stage as Parkinson's disease is frequently seen. A causal therapy is still missing.
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