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1.
Clin Cosmet Investig Dermatol ; 13: 1015-1020, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33380818

RESUMEN

Lipoma belongs to a group of benign mesenchymal tumors. It is in the form of soft masses of adipose tissue encapsulated by a thin layer of fibrous tissue and usually localized subcutaneously. The tumor most often appears in the upper part of the body. Lipomas tend to grow slowly and are small (less than 5cm) lesions. Larger tumors are rare. In this article, we present the case of a patient with a giant head lipoma in the fronto-temporo-parietal region. Both tumor size and location are unique and no such case has been described in the literature so far.

2.
Pharmacol Rep ; 58(6): 955-60, 2006.
Artículo en Inglés | MEDLINE | ID: mdl-17220555

RESUMEN

Overwhelming evidence indicates that nitric oxide (NO) plays an important role in epileptogenesis and seizure activity in the brain. The results of experimental studies on animals provide, however, discrepant information reporting that NO has both anti- and pro-convulsant action in the brain. The objective of this study was to determine the effect of N(G)-nitro-L-arginine (L-NA--a non-specific NO synthase inhibitor) on the anticonvulsant and acute adverse-effect profiles of four second-generation antiepileptic drugs (felbamate [FBM], lamotrigine [LTG], oxcarbazepine [OXC] and topiramate [TPM]) in the maximal electroshock (MES)-induced seizure model and the chimney test in mice. Results indicated that L-NA(at 40 mg/kg, ip) did not affect significantly the antiseizure activity of all examined drugs. However, the antielectroshock action of FBM and LTG after co-administration of L-NA was attenuated by 36% and 28%. In contrast, the anticonvulsant effects of TPM and OXC were almost unchanged after L-NA administration. Moreover, the NO synthase inhibitor (40 mg/kg, ip) did not enhance the acute adverse-effect profiles of the studied antiepileptic drugs in the chimney test. In conclusion, the observed reduction of the anticonvulsant effects of FBM and LTG after co-administration of L-NA may suggest a pro-convulsant activity of L-NA and the cooperation of NO with the antiseizure properties of FBM and LTG in the MES test in mice.


Asunto(s)
Anticonvulsivantes/farmacología , Inhibidores Enzimáticos/farmacología , Óxido Nítrico/fisiología , Nitroarginina/farmacología , Convulsiones/tratamiento farmacológico , Animales , Anticonvulsivantes/efectos adversos , Carbamazepina/análogos & derivados , Carbamazepina/farmacología , Electrochoque , Felbamato , Fructosa/análogos & derivados , Fructosa/farmacología , Lamotrigina , Masculino , Ratones , Oxcarbazepina , Fenilcarbamatos/farmacología , Glicoles de Propileno/farmacología , Topiramato , Triazinas/farmacología
3.
Przegl Lek ; 61(11): 1268-71, 2004.
Artículo en Polaco | MEDLINE | ID: mdl-15727029

RESUMEN

Clinical and experimental data indicate that epilepsy may lead to neuronal death and lesions placed in diverse brain regions. Also, the anticonvulsant activity of some antiepileptic drugs can be impaired in case of neurodegeneration in the brain. The main aim of this review is making a reader familiar with a patomechanism of neurodegeneration as well as the current data concerning the neuro-protective potential of antiepileptic drugs. It is noteworthy that a great number of papers devoted to this problem concern animal models of neurodegeneration produced by either seizure activity or ischemia. Interestingly, there are apparent differences in the direct central effects of antiepileptic drugs in adult and young animals. Majority of antiepileptics at anticonvulsant doses produce massive apoptosis in brains of young rodents, this effect being not present in adult animals. Only topiramate required higher than anticonvulsant doses to induce apoptotic response. Neuroprotective activity in models of ischemia and epilepsy was evident for benzodiazepines (diazepam), lamotrigine, tiagabine, topiramate, and vigabatrin. Recently, topiramate has been documented to exert potent neuroprotective action in human oligodendrocytes exposed to hypoxic-ischemic damage.


Asunto(s)
Anticonvulsivantes/farmacología , Anticonvulsivantes/uso terapéutico , Encéfalo/efectos de los fármacos , Epilepsia/tratamiento farmacológico , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Humanos
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