Mitsuyoshi Sasaki

Co-transfection of EYFP-GH and ECFP-rab3B in an experimental pituitary GH3 cell: a role of rab3B in secretion of GH through porosome

Recently, in order to elucidate the role of rab3B in porosome, we have observed the incorporation of rab3B in the secretion of GH through porosome under confocal laser scanning microscopy (CLSM). Transfected cells with GH-EYFP fusion protein and rab3B-ECFP fusion protein were observed under CLSM, which showed the colocalization of EYFP-GH and ECFP-rab3B in the budding configuration of secretory process. These structural and functional images of rab3B imply the incorporation of rab3B in the secretion of GH through porosome.

Disappearance of gadolinium enhancement in a chemoresistant astrocytoma of the tectum after high-dose interferon beta.

Interferon beta 6 million units per week was administered to a patient with an aggressive astrocytoma in the tectum that was resistant to cisplatin, etoposide, vinblastine, and the oral alkylating agent temozolomide. The tumor was immunopositive for O6-methylguanine-DNA methyltransferase (MGMT). Interferon beta caused the disappearance of the gadolinium-enhanced lesion in the tectum. Interferons have apoptotic and antiangiogenic effects on tumor cells, and the lesions disappearance may have been induced by complexes of these effects. Administration of interferon beta might have a favorable effect on tectal gliomas that are immunopositive for MGMT and resistant to chemoradiotherapy including temozolomide.

Transient Hypotension Induces Remote Neuronal Damage from the Primary Concussion in the Rat

In order to evaluate effects of hypotension in the experimantal concussion model, a conventional fluid percussion method was combined with transient hypotension in the rat. Over the right dorsal cortex, fluid percussion apparatus was located. After the i nsul ts(average 4.3 atm.), venous blood was evacuated until the mean blood pressure fell down to sixty mmHg for six minutes. Sixty minutes after the insults, glucose utilization was studied by 14-C-2-Deoxyglucose (2-DG) method. Other rats were sacrificed under general anesthesia by transcardiac perfusion of 4% paraformaldehyde to make Nissl preparations after twenty four, seventy two hours, or seven days of postinsult survival. Although 2-DG of control group(percussion only) showed normal glucose utilization values, that of hypotension loaded group had hypermatabo 1 ic lesions at the ipsilateral cortex and hippocampus and hypometabo1ic lesions at the ipsilateral basal ggl. The Nissl sections of control group had minor cortical contusion throughout seven days after. Those of hypotension group sacrificed twenty four hours after had the almost same appearance as contol group. But, seventy two hours after, specimens revealed picnotic changes of the ipsilateral cortex and the hippocampus and the depletion of ipsilateral thalamic neurons. Seven days later, these lesions were deteriorated and accompanied by the contralateral cortical neuronal damage. Hypermatabo1ic lesions in 2-DG might be due to the excessive release of excitatory amino acids(EAA), but the neuronal damage was retarded and revealed three days after the insults, which should be one day after in the middle cerebral artery occlusion ischemic model. And the hypometabo1ic lesions also revealed delayed type neuronal damage. According to these results, hypotension could induce delayed neuronal injury in the rat, but 2-DG values of early phase did not fully correspond with the lesion in Nissl preparations. The etiology is unknown but this model wou1d contribute to investigation of the delayed damage after traumatic brain injury.