Fibrillation potentials of denervated rat skeletal muscle are associated with expression of cardiac-type voltage-gated sodium channel isoform Nav1.5.

OBJECTIVE: The molecular mechanisms underlying fibrillation potentials are still unclear. We hypothesised that expression of the cardiac-type voltage-gated sodium channel isoform Nav1.5 in denervated rat skeletal muscle is associated with the generation of such potentials. METHODS: Muscle samples were extracted and analysed biologically from surgically denervated rat extensor digitorum longus muscle after concentric needle electromyographic recording at various time points after denervation (4h to 6days). RESULTS: Both nav1.5 messenger RNA (mRNA) signal on northern blotting and Nav1.5 protein expression on immunohistochemistry appeared on the second day after denervation, exactly when fibrillation potentials appeared. Administration of lidocaine, which has much stronger affinity for sodium channels in cardiac muscle than for those in skeletal muscle, dramatically decreased fibrillation potentials, but had no effect on contralateral compound muscle action potentials. CONCLUSIONS: Expression of Nav1.5 participates in the generation of fibrillation potentials in denervated rat skeletal muscle. SIGNIFICANCE: We proposed an altered expression of voltage-gated sodium channel isoforms as a novel mechanism to explain the occurrence of fibrillation potentials following skeletal muscle denervation.

[Computed tomography (CT) angiography with multidetector row helical CT for detecting spinal dural arteriovenous fistula].

A 59-year-old man had have dysuria and left thigh pain for 2 months. He also experienced transient weakness of both legs twice, which recovered within a few hours. One month ago, he had bowel disturbance. Lumbar MRI showed a swelling of the conus medullaris. Enlarged and tortuous vessels behind the spinal cord on lumbar MRA and CT myelography was demonstrated. Though angiogram through intercostal and lumbar arteries revealed no abnormal findings, CT angiography with multidetector row helical CT (MDCT) showed abnormal vessel in intradural space at sacral level. Angiogram through left internal iliac artery revealed abnormal vessel fed by branches of the lateral sacral artery at the early arterial phase. Thus, diagnosis of dural arteriovenous fistula (DAVF) at the left S1 level was confirmed. It was indicated that CT angiography with MDCT was useful in detecting spinal DAVF especially at sacral level.

[Intermittent intravenous immunoglobulin infusion prevented relapses in patients with remission-exacerbation type chronic inflammatory demyelinating polyradiculoneuropathy].

The intravenous immunoglobulin infusion therapy (IVIg) has recently acquired an important role in the treatment of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Some patients, however, require repetitive infusions to maintain the improvement. We planned a one-day therapy with 0.4 g/kg of IVIg in every 7 or 10 days for two CIDP patients who had required a 5-day course of IVIg in every month because of frequent exacerbations. Serum levels of IgG in both patients were kept as high as 2,000 mg/dl resulting in maintaining the improvement without any side effects.

[Adult onset Langerhans cell histiocytosis with progressive cerebellar ataxia and spastic paraparesis].

A 44-year-old woman with progressive cerebellar ataxia and spastic paraparesis was referred to our hospital. Brain MRI showed bilateral high signals in superior, middle, and inferior cerebellar peduncles on the T2 weighted images. After 3 years, her symptoms progressively worsened in spite of various therapies including whole brain irradiation and high dose oral prednisone. No evidence of diabetes insipidus was noted. In MRI, brainstem lesions expanded to both hemispheres of the cerebellum without enhancement by contrast medium. We confirmed diagnosis of LCH by skin biopsy of intractable truncal rash which emerged after neurological symptoms.

Control mechanism of the circadian clock for timing of cell division in vivo.

Cell division in many mammalian tissues is associated with specific times of day, but just how the circadian clock controls this timing has not been clear. Here, we show in the regenerating liver (of mice) that the circadian clock controls the expression of cell cycle-related genes that in turn modulate the expression of active Cyclin B1-Cdc2 kinase, a key regulator of mitosis. Among these genes, expression of wee1 was directly regulated by the molecular components of the circadian clockwork. In contrast, the circadian clockwork oscillated independently of the cell cycle in single cells. Thus, the intracellular circadian clockwork can control the cell-division cycle directly and unidirectionally in proliferating cells.