Experimental study of perturbative particle transport in the HL-2A tokamak.

Perturbative particle transport experiment has been performed in the HL-2A tokamak by using supersonic molecular beam injection (SMBI) as an external particle source. The spatiotemporal evolution of edge density perturbation is traced and the particle source and the flux-gradient relation are obtained experimentally. The flux-gradient relation is found to be far from the diffusive model and three different transport processes are revealed, including pinch-dominant process, diffusion-pinch process and intermittent decays.

Observation of Double Impurity Critical Gradients for Electromagnetic Turbulence Excitation in Tokamak Plasmas.

The impact of impurity ions on a pedestal has been investigated in the HL-2A Tokamak, at the Southwestern Institute of Physics, Chengdu, China. Experimental results have clearly shown that during the H-mode phase, an electromagnetic turbulence was excited in the edge plasma region, where the impurity ions exhibited a peaked profile. It has been found that double impurity critical gradients are responsible for triggering the turbulence. Strong stiffness of the impurity profile has been observed during cyclic transitions between the I-phase and H-mode regime. The results suggest that the underlying physics of the self-regulated edge impurity profile offers the possibility for an active control of the pedestal dynamics via pedestal turbulence.

[Clinical observation on multiple organ dysfunction syndrome due to fish gall bladder poisoning].

OBJECTIVE: To study the functional changes of liver, kidney, myocardium and gastro-intestine after fish gall bladder poisoning and the pathogenic mechanism of acute renal failure. METHODS: The liver and kidney function, myocardial enzyme, urinary N-acetyl-beta-D-glucosaminidase (N-AG), 24 hrs intake and output volume of liquid and kidney B-ultrasonographic examination in 11 patients of severe acute fish gall bladder poisoning were observed. And kidney biopsy was carried out in one patient under B-ultrasonography for understanding the renal pathological changes. RESULTS: All the 11 patients were cured with disappearance of clinical symptoms. After the poisoning the order of the severity of organ damage were kidney, liver, myocardium and gastro-intestine tract. The levels of blood creatinine, blood urea nitrogen, urinary N-AG, glutamic-pyruvic transaminase, total bilirubin were lowered significantly after treatment. Biopsy examination under light microscope showed toxic damage of renal tubules mainly in proximal tubules, and under electron microscope, the pathologic changes were mitochondrial vacuolar degeneration of tubular epithelial cells, swelling of epithelial cells, partial fusion of processes in glomeruli and narrowing of saccular cavity. CONCLUSION: Fish gall bladder poisoning could cause acute multiple organ dysfunction syndrome (MODS), the affected organs in order of severity of damage were kidney, liver, myocardium and gastro-intestine tract. In kidney the damage was mainly at the proximal tubules. Urinary NAG is a sensitive criterion for determining the diagnosis and prognosis of renal tubular dysfunction.

[Effect of molybdenum Mo on the alkylation of DNA in the liver of rats treated with 14C-diethylnitrosamine].

Effect of molybdenum on the alkylation of DNA in the liver of rats treated with 14C-diethylnitrosamine was studied. When administered orally at a dose of 1 mg/rat/day as (HN4)6 Mo7O24 for 30 days, Mo inhibited the alkylation of DNA in the liver of rats. The level of 3-ethylguanine, N7-ethylguanine and O6-ethylguanine decreased. Simultaneously, the exhalation of 14CO2 and the urinary excretion of 14C- were increased as compared to the controls. At a dose of 5 mg/rat/day, Mo increased the alkylation of DNA in the liver. The amount of 3-ethylguanine, N7-ethylguanine and O6-ethylguanine was higher than that of the controls. The exhalation of 14CO2 and the urinary excretion of 14C- were decreased. The authors believe that the dose of molybdenum is relevant to the role it plays in the carcinogenesis of cell. The role of molybdenum in the carcinogenesis is discussed.