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A 70-year-old female with a history of lobular carcinoma of the breast, status post-mastectomy followed by adjuvant radio-chemotherapy in remission for 4 years was admitted with the features of acute liver failure (ALF). Iron studies revealed a hemochromatosis picture and the CT and MRI scans of the abdomen suggested cirrhosis. An extensive workup failed to identify an etiology. A trans-jugular liver biopsy was obtained and revealed poorly differentiated carcinoma consistent with the metastasis of breast primary. The patient's condition deteriorated and died within a week following the onset of acute hepatic failure. DNA testing revealed that the patient was heterozygous for H63D mutation. In cases of ALF with the suspicion of malignancy, liver biopsy should be obtained to evaluate an infiltrative hepatic disease., (© The Author(s) 2020. Published by Oxford University Press.)

The effects of pyrroloquinoline quinone (PQQ) and coenzyme Q(10) (Co Q(10)), either alone or together, on the learning ability and memory function of rats were investigated. Rats fed a PQQ-supplemented diet showed better learning ability than rats fed a CoQ(10)-supplemented diet at the early stage of the Morris water maze test. The combination of both compounds resulted in no significant improvement in the learning ability compared with the supplementation of PQQ alone. At the late stage of the test, rats fed PQQ-, CoQ(10)- and PQQ + CoQ(10)-supplemented diets showed similar improved learning abilities. When all the groups were subjected to hyperoxia as oxidative stress for 48 h, rats fed the PQQ- and CoQ(10) supplemented diets showed better memory function than the control rats. The concurrent diet markedly improved the memory deficit of the rats caused by oxidative stress. Although the vitamin E-deficient rats fed PQQ or CoQ(10) improved their learning function even when subjected to hyperoxia, their memory function was maintained by PQQ rather than by CoQ(10) after the stress. These results suggest that PQQ is potentially effective for preventing neurodegeneration caused by oxidative stress, and that its effect is independent of either antioxidant's interaction with vitamin E.