Posttraumatic hemidystonia treated with unilateral globus pallidus interna stimulation: Long-term follow-up and radiologic features.

OBJECTIVE: Hemidystonia is a unilateral clinical presentation of dystonia, and it is usually refractory to current methods of medical treatment. Recently, deep brain stimulation has given some hope of recovery to dystonic patients. MATERIALS AND METHODS: A 30-year-old right-handed man with no abnormal perinatal history or family history of movement disorders was admitted to our institution. The patient had suffered right-sided dystonia for more than three years after severe head trauma sustained four years prior. RESULTS: We performed a stereotactic implantation of an electrode into the left globus pallidus internus (GPi) and he showed excellent response to pallidal stimulation during long-term follow-up. CONCLUSIONS: We present a unique case of secondary posttraumatic hemidystonia treated with contralateral GPi stimulation with an excellent outcome. Pallidal stimulation can be a good treatment option for posttraumatic hemidystonia in selected cases.

Health information system based on EHR for workplace health promotion.

The multifactoral origins of occupational health, must take into consideration of all factors simultaneously, including the working environment,lifestyle habits and medical examinations. We defined the concepts and requirements of the 'workplace electronic health records' (WEHR). Hereby, we present the architecture and function of health information system (HIS) based on WEHR for workplace health promotion (WHP).

Monensin-mediated growth inhibition in acute myelogenous leukemia cells via cell cycle arrest and apoptosis.

Monensin, an Na(+) ionophore, regulates many cellular functions including apoptosis. However, there has been no report about the antitumoral effect of monensin on acute myelogenous leukemia (AML). Here, we investigated the antiproliferative effect of monensin on AML cells in vitro and in vivo. Monensin efficiently inhibited the proliferation of all of 10 AML cell lines, with IC(50) of about 0.5 microM. DNA flow cytometric analysis indicated that monensin induced a G(1) and/or a G(2)-M phase arrest in these cell lines. To address the mechanism of the antiproliferative effect of monensin, we examined the effect of monensin on cell cycle-related proteins in HL-60 cells. The levels of CDK6, cyclin D1 and cyclin A were decreased. In addition, monensin not only increased the p27 level but also enhanced its binding with CDK2. Furthermore, the activities of CDK2- and CDK6-associated kinases reduced by monensin were associated with hypophosphorylation of Rb protein. Monensin also induced apoptosis in AML cells including HL-60 cells. The apoptotic process of HL-60 cells was associated with changes in Bax, caspase-3, caspase-8 and mitochondria transmembrane potential (Deltapsi(m)). In particular, monensin (i.p. at a dose of 8 mg/kg thrice weekly) significantly reduced the tumor size of BALB/c mice that were inoculated s.c. with its derived cell line, WEHI-3BD cells (69% growth inhibition relative to control group; p < 0.05). Tumors from monensin-treated mice exhibited increased apoptosis, and these tumor were immunohistochemically more stained with Bax, Fas and p53 antibodies than control tumors. In conclusion, this is the first report that monensin potently inhibits the proliferation of AML cells.