Role of p53 in neurotoxicity induced by the endoplasmic reticulum stress agent tunicamycin in organotypic slice cultures of rat spinal cord.

The endoplasmic reticulum (ER) is important for maintaining the quality of cellular proteins. Various stimuli can disrupt ER homeostasis and cause the accumulation of unfolded or misfolded proteins, i.e.

The effects of neuronal induction on gene expression profile in bone marrow stromal cells (BMSC)--a preliminary study using microarray analysis.

Bone marrow stromal cells (BMSC) have been anticipated as a donor for cell type for transplantation therapy in various neurological disorders. However, their neurogenic capacity still remains undetermined. In this study, we aimed to clarify whether in vitro chemical treatment promotes their neuronal differentiation on the level of gene expression.

Proteasome inhibition induces selective motor neuron death in organotypic slice cultures.

A dysfunctional ubiquitin-proteasome system recently has been proposed to play a role in the pathogenesis of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). We have shown previously that spinal motor neurons are more vulnerable to proteasome inhibition-induced neurotoxicity, using a dissociated culture system. To confirm this toxicity, we used organotypic slice cultures from rat neonatal spinal cords, which conserve the structure of the spinal cord in a horizontal plane, enabling us to identify motor neurons more accurately than in dissociated cultures.

Glycation--a sweet tempter for neuronal death.

Glycation, one of the post-translational modifications of proteins, is a nonenzymatic reaction initiated by the primary addition of a sugar aldehyde or ketone to the amino groups of proteins. In the early stage of glycation, the synthesis of intermediates leading to the formation of Amadori compounds occurs. In the late stage, advanced glycation end products (AGE) are irreversibly formed after a complex cascade of reactions.

Effect of proteasome inhibitor on cultured mesencephalic dopaminergic neurons.

Proteasomal dysfunction has been implicated in the pathogenesis of Parkinson's disease (PD). We examined the effect of a selective proteasomal inhibitor, epoxomicin, on primary cultured mesencephalic neurons. Exposing rat cultured mesencephalic neurons to epoxomicin for 24 h resulted in neurotoxicity in a dose-dependent manner.

Brefeldin A-induced neurotoxicity in cultured spinal cord neurons.

Brefeldin A (BFA) is a fungus metabolite that is known to cause the disassembly of the Golgi complex and apoptosis in exposed cells, both of which have been suggested as playing roles in the pathogenesis of neurodegenerative diseases, particularly amyotrophic lateral sclerosis (ALS). This study showed that BFA caused neurotoxicity and apoptotic nuclear changes in cultured spinal neurons of rat spinal cord in a dose- and time-dependent manner. The spinal motor neurons were more vulnerable to this neurotoxicity.

Cervical myelopathy due to a "tight dural canal in flexion" with a posterior epidural cavity.

A 41-year-old man noticed weakness and atrophy in his right hand and forearm resembling the non-progressive juvenile muscular atrophy of unilateral upper extremity (Hirayama's disease). MRI showed an abnormal cavity in the posterior epidural space which appeared on neck flexion communicating with the subarachnoid space in addition to the flattening of the lower cervical spinal cord on neck flexion. When evaluating atypical cases of Hirayama's disease, the pathomechanism demonstrated in the present case should be taken into consideration.

Intracranial hemorrhage in neuro-Behçet's syndrome.

Objective: Most cerebrovascular disturbances in Behçet's syndrome are occlusive in nature, while hemorrhage is rare. In this paper, we report three cases of neuro-Behçet's syndrome presenting with intracerebral hemorrhaging, and discuss the possible causes as they relate to cyclosporine treatment.

Patients: Three cases of neuro-Behçet's syndrome presented with intracranial hemorrhage.

Detection of N epsilon-(carboxymethyl)lysine (CML) and non-CML advanced glycation end-products in the anterior horn of amyotrophic lateral sclerosis spinal cord.

Introduction: The involvement of glycation in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS) was recently indicated. We previously reported the existence of an Amadori product, 1-hexitol-lysine (1-HL), which is formed in the early glycation reaction, in axonal spheroids of the anterior horn of the ALS spinal cord.

Objective: The purpose of the present study was to confirm the occurrence of the later-stage glycation reaction that follows the early glycation reaction and leads to the formation of advanced glycation end products (AGEs).

Effect of geranylgeranylaceton on cellular damage induced by proteasome inhibition in cultured spinal neurons.

We investigated the effect of two proteasome inhibitors, lactacystin and epoxomicin, on cultured spinal cord neurons. The incubation of spinal neurons with proteasome inhibitors for 24 hr induced neurotoxicity in a dose-dependent manner. We found motor neurons to be more vulnerable to proteasome-induced neurotoxicity than nonmotor neurons.