Direct observation of imploded core heating via fast electrons with super-penetration scheme.

Fast ignition (FI) is a promising approach for high-energy-gain inertial confinement fusion in the laboratory. To achieve ignition, the energy of a short-pulse laser is required to be delivered efficiently to the pre-compressed fuel core via a high-energy electron beam. Therefore, understanding the transport and energy deposition of this electron beam inside the pre-compressed core is the key for FI. Here we report on the direct observation of the electron beam transport and deposition in a compressed core through the stimulated Cu Kα emission in the super-penetration scheme. Simulations reproducing the experimental measurements indicate that, at the time of peak compression, about 1% of the short-pulse energy is coupled to a relatively low-density core with a radius of 70 µm. Analysis with the support of 2D particle-in-cell simulations uncovers the key factors improving this coupling efficiency. Our findings are of critical importance for optimizing FI experiments in a super-penetration scheme.

Insufficient ex vivo expansion of Valpha24(+) natural killer T cells in malignant lymphoma patients related to the suppressed expression of CD1d molecules on CD14(+) cells.

BACKGROUND: Valpha24(+) natural killer T (NKT) cell is a human counterpart of mice Valpha14(+) NKT cell that has a regulatory role for innate and acquired potential antitumor activity. The efficient expansion of NKT cells is an obstacle to the clinical application of Valpha24(+) NKT cells for immunotherapy. METHODS: We used mononuclear cells (MNC) obtained from the peripheral blood (PB) of normal healthy donor (HD) and malignant lymphoma (ML) patients before and after granulocyte colony-stimulating factor (G-CSF) treatment. MNC were cultured for 12 days with alpha-galactosylceramide (100 ng/mL) and interleukin-2 (IL-2; 100 U/mL). RESULTS: The fold expansion of Valpha24(+) NKT cells was higher in HD than in ML patients (208 versus 0.00), despite comparable numbers of Valpha24(+) NKT cells before culture. G-CSF administration enhanced the predominance of Valpha24(+) NKT cell fold expansion in HD compared with ML patients (1935 versus 1.95). After treatment with G-CSF, the expression of CD1d molecules was up-regulated in CD14(+) cells from HD but not ML patients. The fold expansion of Valpha24(+) NKT cells and CD1d expression on CD14(+) cells was strongly correlated in both HD and ML patients (r(2)=0.84). However, replacement of a patient's CD14(+) cells with HD cells did not increase the efficacy of Valpha24(+) NKT cell expansion. DISCUSSION: G-CSF-mobilized PB from ML patients has inhibitory characteristics for Valpha24(+) NKT cell expansion as a result of both monocytes and Valpha24(+) NKT cells. Multiple procedures would be needed for the expansion of patients' Valpha24(+) NKT cells.

Congenital unilateral hydrocephalus.

An 848-g infant delivered after a 30-week gestation had been diagnosed by ultrasonic examination as having a unilateral ventriculomegaly from the 29th week of gestation. Computerized tomography (CT) demonstrated a greatly dilated right lateral ventricle with no apparent space-occupying lesion within the ventricle and no passage of the contrast medium (metrizamide) through the foramen of Monro. The child was diagnosed as having unilateral hydrocephalus due to congenital obstruction of the foramen and underwent a ventriculoperitoneal shunt operation on day 49 (37 weeks and 5 days of amended gestation age; 1,420 g body weight). The postoperative course was uneventful and the patient was discharged on day 126 with no marked developmental retardation. Angiography carried out at 8 months postpartum revealed displacement and hypoplasia of the deep cerebral veins. The pathogenesis and treatment of unilateral hydrocephalus are discussed.