A Neurotoxocariasis Case Manifesting Multiple Cerebral Infarction and Eosinophilic Meningoencephalitis

Although Toxocara canis is known to cross the blood-brain barrier, central nervous system involvement is uncommon. Clinical manifestations vary and include cerebral infarction, meningoencephalitis, myelitis, vasculitis or seizure. However cerebral infarction and meningoencephalitis rarely occur simultaneously. We report a case of multiple cerebral infarction combined with eosinophilic meningoencephalitis in a patient with neurotoxocariasis. After control of increased intracranial pressure and treatment with albendazole and steroid, the patient’s clinical symptoms improved markedly.

Recurrent Falls Associated with Lower Limb Deep Vein Thrombosis

No abstract available.

Inhibitory Effect of 3,4,5-Tricaffeoylquinic Acid on Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Apoptosis

BACKGROUND: 1-Methyl-4-phenylpyridinium (MPP+) causes a neuronal cell injury that is similar to the findings observed in Parkinson's disease. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. Nevertheless, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the neuronal cell death due to exposure of parkinsonian toxin MPP+ remains unclear. METHODS: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death in relation to apoptotic process was examined. RESULTS: MPP+ induced a decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increase in the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in the apoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. 3,4,5-Tricaffeoylquinic acid attenuated another parkinsonian neurotoxin rotenone-induced cell death. CONCLUSIONS: 3,4,5-Tricaffeoylquinic acid may attenuate the MPP+-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems to be ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.