Brain metastasis from malignant fibrous histiocytoma of the heart: case report

This is the second reported case of a malignant fibrous histiocytoma of the heart that metastasized to the brain. A 33-year-old woman developed headache, nausea, and ataxic gait 9 months after removal of the tumor from the left atrium of the heart. Computed tomographic and magnetic resonance imaging scans disclosed multiple metastatic tumors in the brain. Although dramatic improvement in her symptoms and signs followed the removal of the brain tumors, she died of tumor recurrence in the left atrium 3 months after the removal of the metastatic brain tumors.     

Preparation and Characterization of a Murine Monoclonal Antibody (MDR3M) Reactive with mdr3 Gene Product

A murine monoclonal antibody (MDR3M) (isotype: IgM) reactive with mdr3 gene product was generated by immunizing mice with mdr3 -specific peptide (H₂N-¹²WRPTSAEGDFELGISSKQKRKKTKTVKMI⁴¹G-COOH) and hybridizing the primed mouse splenic B cells with X63-Ag8,6.5.3 mouse plasmacytoma cells. MDR3M did not cross-react with mdr1 gene product. This monoclonal antibody may be useful for analyzing the role of mdr3 gene product in cells and tissues.     

Marked improvement of delayed methotrexate-induced leukoencephalopathy treated with high-dose folinic acid

We report the case of a patient with delayed methotrexate (MTX)-induced leukoencephalopathy who showed a marked improvement both in clinical and neuroimaging findings after a high-dose of the active form of folinic acid (leucovorin) treatment. The patient developed progressive affective impairment accompanied by headache, nausea and vomiting after treatment with MTX during the chemotherapy for acute lymphoblastic leukemia, and diagnosed as delayed type MTX-induced leukoencephalopathy. After an intravenous injection of high-dose folinic acid (total 1920 mg), neurological deficits and white matter changes dramatically improved in a few weeks. Although delayed MTX-induced leukoencephalopathy may cause irreversible brain damage, an early treatment with high dose leucovorin may thus facilitate the marked improvement of clinical findings and white matter abnormalities.     

Olfactory dysfunction in Parkinson's disease

Journal of Neurology - Olfactory dysfunction in Parkinson's disease (PD) has been described for more than thirty years and known as one of the commonest non-motor symptoms in PD. Recently, it...     

Intracranial arterial vasospasm associated with pituitary apoplexy after head trauma--case report.

A case of intracranial arterial vasospasm caused by pituitary apoplexy after head trauma is reported. In this case, pituitary apoplexy was secondary to head trauma, and the vasospasm was thought to be due to subarachnoid hemorrhage from a pituitary tumor. No such case has previously been reported in the literature.     

Induction of NADPH-diaphorase activity in the hippocampus in a rat model of cerebral ischemia and ischemic tolerance

Preconditioning of the brain with sublethal ischemia induces tolerance to subsequent lethal periods of ischemia (ischemic tolerance). In this study, we used NADPH-diaphorase histochemistry to investigate the postischemic changes of nitric oxide synthase (NOS) in the hippocampus in a rat model of cerebral ischemia and ischemic tolerance. Forebrain ischemia was induced by 4-vessel occlusion for 3 min as an ischemic preconditioning. Three days after the preconditioning or sham operation, second ischemia was induced for 6 min. A transient increase in NADPH-diaphorase activity, beginning after 2 h and maximal after 1 day, was observed in CA1 pyramidal neurons of rats subjected to 3 min of preconditioning ischemia as well as 6 min of subsequent ischemia both with and without preconditioning. In addition, expression of NADPH-diaphorase activity was seen in reactive glial cells in the damaged CA1 region of animals subjected to 6 min of ischemia without preconditioning. Thus, direct involvement of increased NADPH-diaphorase activity in ischemic tolerance was not suggested because the increased NADPH-diaphorase activity preceded the induction of ischemic tolerance which takes place 1–7 days after preconditioning. However, the present findings suggest that the induction of neuronal NADPH-diaphorase activity occurs in response to cerebral ischemia.     

Sequential changes of [H]forskolin, [H]cyclohexyladenosine and [H]PN200-110 binding sites in the brain of 6-hydroxydopamine-lesioned rats

Receptor autoradiographic technique was studied to investigate sequential changes in adenylyl cyclase, adenosine A1 receptors and L-type calcium channels in the striatum and substantia nigra 1-8 weeks after unilateral 6-hydroxydopamine injection of the medial forebrain bundle in rats. [3H]Forskolin, [3H]cyclohexyladenosine (CHA) and [3H]PN200-110 were used to label adenylyl cyclase, adenosine A1 receptors and L-type calcium channels, respectively. The degeneration of the nigrostriatal pathway caused a significant increase in [3H]forskolin binding in the striatum of both the ipsilateral and contralateral sides from 2 to 4 weeks post-lesion. The ipsilateral substantia nigra showed a transient increase in [3H]forskolin binding 4 weeks post-lesion. In contrast, [3H]CHA binding showed no significant change in most brain areas after lesioning. On the other hand, a conspicuous decrease in [3H]PN200-110 binding was observed in the dorsolateral striatum of ipsilateral side 4 weeks post-lesion. Thereafter, the striatum of both the ipsilateral and contralateral sides showed a significant decrease in [3H]PN200-110 binding 8 weeks post-lesion. These results demonstrate that unilateral 6-hydroxydopamine into the medial forebrain bundle of rats can experimentally cause a significant increase in adenylyl cyclase binding sites in the striatum and substantia nigra, whereas no conspicuous change in adenosine A1 receptors is observed in these areas during post-lesion. In contrast, L-type calcium channels were progressively damaged in the striatum after unilateral 6-hydroxydopamine treatment. These findings suggest that adenylyl cyclase and calcium system may contribute to the degeneration processes of the dopaminergic neurones.     

Linear antigenic regions of the structural proteins of human T-cell lymphotropic virus type I detected by enzyme-linked immunosorbent assays using synthetic peptides as antigens.

We synthesized 46 sequential peptides 21 to 39 amino acids long over the structural protein of human T-cell leukemia virus type I (HTLV-I; the p19 and p24 gag protein and the gp46 and p20E env proteins) and tested their reactivities against antibodies in sera from HTLV-I healthy carriers and patients diagnosed as having human T-cell leukemia-lymphoma (ATLL) and myelopathy (HAM) by using an enzyme-linked immunosorbent assay. Of the 46 synthetic peptides, 18 peptides (2 corresponding to the p19 gag protein, 2 corresponding to the p24 gag protein, 8 corresponding to the gp46 env protein, and 6 corresponding to the p20E env protein) reacted with antibodies in the sera from HTLV-I healthy carriers. In particular, the peptides comprising amino acids 100 to 119 and 119 to 130 of the gag and 175 to 199, 213 to 236, 253 to 282, and 288 to 317 of the env proteins reacted with antibodies in sera from more than 30% of HTLV-I healthy carriers. These peptides also showed high reactivities to the antibodies in the sera from patients with ATLL and HAM. The results indicate that the predominant antigenic regions of the structural protein of HTLV-I were located at the C-terminal end of the p19 gag protein and the C-terminal half of the gp46 env protein, and the corresponding peptides proved to be useful antigens in detecting antibodies in the sera from individuals infected with HTLV-I.     

A case of intramural uterine stromal tumor with epithelial differentiation.

A case of intrauterine tumor in a 62-year-old Japanese woman is presented. It was thought initially that this was a case of uterine tumor resembling an ovarian sex cord tumor. To examine the cytological features of the tumor cells, electron microscopical and immunohistochemical studies were done, and a hormone assay of the tumor tissue was performed. The tumor cells were rich in rough endoplasmic reticulum (rER), mitochondria and microfilaments. Some tumor cells tended to form glandular patterns, but these epithelial elements were frequently scattered among fibrous stromal elements. Though many tumor cells with an epithelial appearance possessed a large quantity of cytokeratin and vimentin, they did not secrete estradiol, progesterone, testosterone or human chorionic gonadotropin. This case was finally diagnosed as an intramural uterine stromal tumor with epithelial differentiation after taking all the available data into consideration. This would be classified as an endometrial stromal tumor with epithelial elements, recently proposed and named by Clement and Scully.