用混合粘合剂碳糊电极测定丁螺环酮

用混合粘合剂碳糊电极测定丁螺环酮张正奇，曾鸽鸣，刘传桂，黎艳飞（湖南大学化学化工系，长沙４１００８２）碳糊电极无毒，制作方便，表面更新容易，应用电位范围广，在药物分析中已有应用［１～５］。我们在液体石腊中加入添加剂，组成混合粘合剂，可显著改善电极的检...     

Proposal of a dose-response relationship between aluminium welding fume exposure and effect on the central nervous system.

Exposure to high levels of aluminium can affect the human central nervous system. Abnormalities of psychomotor function have been observed among haemodialysis patients with mean aluminium concentrations in serum of about 60 micrograms/l. According to our own data this corresponds to a urinary level of about 330 micrograms Al/l in aluminium-exposed welders without kidney failure. This post-shift urinary level of aluminium is estimated to be attained after 40 years of exposure to a welding fumes at an environmental concentration of approximately 1.6 mg/m3 of aluminium. An increased prevalence of effects on the nervous system was observed among welders exposed to aluminium fumes for more than 13 years. This finding supports the concept of cumulative toxicity due to aluminium exposure. On the basis of these observation, we suggest that the level of aluminium in welding fumes should not exceed 1 mg/m3.     

Decreased glomerular filtration rate in solderers exposed to cadmium.

OBJECTIVES--to evaluate the degree of cadmium induced glomerular impairment and to assess the dose-response relation between cadmium dose and the prevalence of glomerular dysfunction. METHODS--A comparison of glomerular filtration rates (GFR) assessed by Cr-EDTA clearance was made in 42 solderers previously exposed to cadmium for at least five years. Blood and urine data were collected at health examinations in 1984, 1989, and 1993. Individual doses of cadmium were estimated by analysing cadmium in blood. RESULTS--Glomerular lesions induced by cadmium are irreversible and the GFR decreases with the degree of tubular damage. The GFR also decreases with cadmium dose and there is a dose-response relation between blood cadmium and prevalence of glomerular damage with 3.4% prevalence at blood cadmium concentrations below 50 nmol/l, 33% at blood cadmium concentrations between 50 and 75 nmol/l and 100% prevalence of glomerular damage when cadmium in blood exceeds 75 nmol/l. CONCLUSIONS--The kidney lesions induced by cadmium are irreversible and the prevalence of those lesions are dose dependent. There is also evidence of a dose related decrease in GFR even a long time after the end of exposure. Exposure to cadmium should therefore be minimised and workers exposed to cadmium should be examined regularly for many years after the end of exposure.     

Viral infections in the mouth

Oral hairy leukoplakia (OHL) and Kaposi's sarcoma (KS) are commonly encountered in the HIV-infected patient. A unique feature of OHL is non-cytolytic high level of replication of Epstein–Barr virus (EBV) in the glossal epithelium. The expression of viral-encoded anti-apoptotic proteins concomitant to replicative proteins probably underlies this phenomenon. The question of whether OHL arises from activation of EBV latent in the tongue, or from superinfection by endogenous EBV shed via non-glossal sites or by exogenous EBV remains unresolved. Human herpesvirus 8 (HHV8) is now seen as necessary but not sufficient cause of KS. Expression of HHV8-encoded oncogenic proteins in endothelial cells probably explains the aberrant proliferation of these cells in KS lesions. Studies into why KS is so commonly observed at the palate in HIV-infected patients may provide important clues to its pathogenesis.     

Effects of THA on ionic currents in myelinated axons of Xenopus laevis

In voltage-clamp experiments with the myelinated nerve fibre of Xenopus laevis, 9-amino-1,2,3,4-tetrahydroacridine (THA) decreased both Na+ and K+ currents and shifted the steady state inactivation potential curve in a negative direction. The effects may be described as (a) a decrease of the permeability constant PNa, (b) a modified potential dependence of the inactivating system and (c) a decrease of PK. The Na+ system was affected more than the K+ system.     

Conceptual problems in establishing the critical concentration of cadmium in human kidney cortex

The definition of the "critical concentration" for cadmium is compared with the concepts used to establish this measure in some recent publications. The term has not been clearly defined on a population basis and this has given rise to certain confusion. Different groups of investigators therefore have arrived at different estimates of the "critical concentration" for cadmium in human kidney cortex. A new measure, the "population critical concentration" (PCC) with a clearly defined response rate, is suggested. A reanalysis of the published data indicates that the PCC-10 (10% response rate) for cadmium in kidney cortex is likely to be in the range 180-220 micrograms/g and the PCC-50 is likely to be about 25% higher.     

The applicability of the measurement of urinary thioethers

Summary The excretion of thioethers was measured in the urine of 6 volunteers, who were experimentally exposed to styrene, and 18 styrene workers. In addition, 12 clerks (non-smokers) and 12 sheet-metal workers (smokers) served as control groups. Diet was standardized during the experiments. Thioethers were measured by a spectrophotometric method. The volunteers were exposed to styrene, 210 mg/m³, for 2 h at a 50-W workload. An increase in thioether excretion was observed; the largest was in the urine samples collected between 0.5 and 5 h after the end of the exposure. After 43 h the excretion of thioethers was close to the preexposure level (3.5 mmol/mol creatinine). About 1% of the styrene absorbed was detected as thioethers in urine, which is only about 1/10 of the conversion reported for rats. From excretion rate curves a half-life of about 11 h was calculated for styrene thioethers. The styrene workers were employed at two plants. The average exposure to styrene (time-weighted average 8 h) was estimated to be about 115 mg/m3 (smokers in plant A), 55 mg/m³ (non-smokers in plant A) and 10 mg/m³ (non-smokers in plant B). The excretion of thioethers in exposed workers at plant A was higher by 2–4 mmol/mol creatinine than that in non-exposed controls. In plant B, where exposure was lower, an increase in that amount of thioethers excreted in the urine by exposed workers was less pronounced, and was statistically significant only when post-shift samples were compared with pre-shift samples. The results of the present study indicate that control samples should be collected both from non-exposed groups and from the exposed individuals before work shifts, to improve the likelihood of detecting genotoxic exposure in the work environment.