Measurement of axonal excitability: Consensus guidelines.

Measurement of axonal excitability provides an in vivo indication of the properties of the nerve membrane and of the ion channels expressed on these axons. Axonal excitability techniques have been utilised to investigate the pathophysiological mechanisms underlying neurological diseases. This document presents guidelines derived for such studies, based on a consensus of international experts, and highlights the potential difficulties when interpreting abnormalities in diseased axons.

[Trial of rituximab in three patients with neuromyelitis optica].

Patients with relapsing neuromyelitis optica (NMO) showing contiguous long spinal cord lesions extending over three vertebral segments on the MRI and with positive anti-aquaporin 4 antibodies in sera are usually treated with glucocorticoids or azathioprine. However, some NMO patients even after adequate treatments show relapses. Rituximab (anti-CD 20) therapy has recently been reported to inhibit relapses.

A case of epileptic negative myoclonus: therapeutic considerations.

This study presents a patient with epileptic negative myoclonus who showed interictal focal epileptic discharges in the centrotemporal region. The patient's seizures were exacerbated by carbamazepine, zonisamide, and valproate, but completely controlled by ethosuximide, and were suggested to have some relation with thalamocortical oscillation mechanisms. Ethosuximide is supposed to be a drug of worth to try to use in epileptic negative myoclonus patients with centrotemporal spike foci.

[Clinical evaluation of serum cytokine from patients with collagen diseases].

Purpose: Systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS) are characterized by an imbalance of cytokine production. To clarify the relationship between the profile of cytokines and the pathophysiology of systemic autoimmune diseases, we estimated the cytokine levels in sera from patients with several systemic autoimmune diseases.

Method: Serum cytokine levels in patients with unclassified connective tissue diseases were measured using ultrasensitive specific enzyme-linked immunosorbent assay (ELISA).

Pineal dermoid cyst developing 18 years after gross total removal of a pineal mature teratoma.

A 21-year-old male presented with a pineal dermoid cyst manifesting as headache and diplopia. He had undergone gross total removal of a pineal mature teratoma 18 years before and had done well until recently. Diffusion-weighted magnetic resonance imaging showed a region of high signal intensity due to a round mass in the pineal region and extending into the trigone of the right lateral ventricle.

[An imbalance between Th1 and Th2-like cytokines in patients with autoimmune diseases--differential diagnosis between Th1 dominant autoimmune diseases and Th2 dominant autoimmune diseases].

An imbalance between T helper cell (Th)1 and Th2-like cytokines has been described in several autoimmune diseases. Organ specific autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel diseases (IBD) are caused by Th1 dominant immune responses. On the contrary, systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome(SS) are characterized by Th2 dominant imbalance of cytokine production.

Tumor necrosis factor-alpha induces p53-dependent apoptosis in rat glioma cells.

In this study, we demonstrated that tumor necrosis factor (TNF)-alpha inhibited the viability of rat glioma (C6) cells and induced apoptosis but did not affect the viability of rat newborn brain, mainly astroglial cells. The antitumor activity of TNF-alpha against C6 cells was partially inhibited by actinomycin D and cycloheximide, suggesting that it is possibly dependent upon new ribonucleic acid and protein synthesis. The results of immunoblotting assay demonstrated that TNF-alpha decreased the expression of mutant p53 protein but induced the expression of wild-type p53 in C6 cells during apoptosis.

Combination therapy with cisplatin and nifedipine inducing apoptosis in multidrug-resistant human glioblastoma cells.

The authors found that multidrug-resistant human glioblastoma GB-1 cells demonstrated significantly more resistance to cisplatin than did nondrug-resistant human glioblastoma U87-MG cells (p < 0.1). They therefore attempted to determine whether calcium channel blockers enhance the antitumor activity of cisplatin against GB-1 cells.

Combination therapy with cisplatin and nifedipine induces apoptosis in cisplatin-sensitive and cisplatin-resistant human glioblastoma cells.

We attempted to determine whether calcium channel blockers (CCBs) enhance the anti-tumour activity of cis-diamminedichloroplatinum (cisplatin) against both cisplatin-sensitive human glioblastoma U87 MG cells and cisplatin-resistant U87-MG-CR cells, the latter of which we developed for resistance to cisplatin. Nifedipine, a dihydropyridine class CCB, significantly enhanced the anti-tumour effect of cisplatin on these two cell types in vitro and in vivo. Our findings also indicated that, in the absence of normal extracellular Ca2+ nifedipine was capable of enhancing the cytotoxicity of cisplatin.

bcl-2 gene enables rescue from in vitro myelosuppression (bone marrow cell death) induced by chemotherapy.

Recent studies have shown that the use of cytokines such as granulocyte colony-stimulating factor (G-CSF) to ameliorate chemotherapy-induced myelosuppression may enhance the viability of tumour cells with functional receptors for these cytokines. In this study, therefore, we used murine bone marrow (BM) cells in an in vitro model in an attempt to determine whether topoisomerase inhibitors (camptothecin, etoposide and doxorubicin) induce myelosuppression (BM cell death) and whether novel treatments other than the administration of G-CSF can be used for rescue from myelosuppression. DNA fragmentation assay, ultrastructural analysis and cell cycle analysis demonstrated that these chemotherapeutic agents induced apoptosis in BM cells.

bcl-2 gene prevents apoptosis of basic fibroblast growth factor-deprived murine aortic endothelial cells.

Growth factors such as basic fibroblast growth factor (bFGF) have been found to promote the survival and proliferation of endothelial cells. However, the mechanism by which growth factors control the regeneration and degeneration of the endothelial cells remained poorly understood. In this study, we demonstrated that apoptosis of murine aortic endothelial (MAE) cells was induced by deprivation of bFGF but required new RNA and protein synthesis.

Transfection with a bcl-2 expression vector protects transplanted bone marrow from chemotherapy-induced myelosuppression.

The use of cytokines such as granulocyte-colony-stimulating factor (G-CSF) to ameliorate chemotherapy-induced myelosuppression may not only stimulate the recovery of normal hematopoietic cells but may also enhance the proliferation of the tumor cells with functional receptors for these cytokines. In this study, we show that administration of recombinant human (rh) G-CSF decreased the in vitro and in vivo cytotoxic effects of Adriamycin or etoposide on L1210 murine leukemic cells with receptors for rhG-CSF. Transplantation of bone marrow cells expressing high levels of bcl-2 from a retroviral construct [MPZenNeo(bcl-2)] (bcl-2-BMT) did not decrease the in vivo cytotoxic effect of etoposide on L1210 cells, but enabled recovery of myelopoiesis following etoposide-induced myelosuppression to almost the same extent as did the administration of rhG-CSF.

Induction of apoptosis in murine ACTH-secreting pituitary adenoma cells by bromocriptine.

Bromocriptine, a dopamine agonist, is now an accepted primary therapeutic agent for patients with prolactinomas and other pituitary adenomas. In this study, we demonstrated that bromocriptine inhibited the proliferation of murine ACTH-secreting pituitary adenoma (AtT-20) cells. In addition, the antitumor activity of bromocriptine was inhibited both by actinomycin D and cycloheximide, suggesting that it was dependent on new RNA and protein synthesis.

Preoperative embolization of meningiomas: its efficacy and histopathological findings.

This report deals with the operative and histopathological findings in 14 meningiomas of 13 patients who were subjected to preoperative embolization. This procedure facilitated the removal of 11 of the 14 tumors and minimized blood loss. In the majority of cases the following histopathological findings were documented: 1) Presence of emboli and thrombi within the tumor and/or dural vessels; 2) associated vascular thrombosis; 3) ischemic changes of the tumor cells; 4) pathologic evidence of infarction with or without inflammatory response, and 5) diffuse or nodular necrosis and surviving tumor cell clusters with an island-like appearance.

Induction of apoptosis in rat somatotrophin-secreting pituitary adenoma cells by bromocriptine.

Bromocriptine, a dopamine agonist, is now an accepted primary therapeutic agent for patients with prolactinomas and other pituitary adenomas. In this study, we demonstrated that bromocriptine inhibited the proliferation of rat somatotrophin-secreting pituitary adenoma (GH1) cells. In addition, the antitumor activity of bromocriptine was inhibited both by actinomycin D and cycloheximide, suggesting that it was dependent upon new RNA and protein synthesis.

[A retrospective group study on post-thymectomy myasthenia gravis].

Retrospective group study on post-thymectomy myasthenia gravis (post-Tm MG) was carried out. Five hundred and twenty-seven resected thymoma cases (133 cases with MG and 394 cases without MG) were collected from 9 hospitals. Post-Tmx MG occurred in 18 out of 394 cases -4.