The development of involuntary and voluntary attention from childhood to adulthood: a combined behavioral and event-related potential study.

OBJECTIVE: This study investigated auditory involuntary and voluntary attention in children aged 6-8, 10-12 and young adults. The strength of distracting stimuli (20% and 5% pitch changes) and the amount of allocation of attention were varied. METHODS: In an auditory distraction paradigm event-related potentials (ERPs) and behavioral data were measured from subjects either performing a sound duration discrimination task or watching a silent video. RESULTS: Pitch changed sounds caused prolonged reaction times and decreased hit rates in all age groups. Larger distractors (20%) caused stronger distraction in children, but not in adults. The amplitudes of mismatch negativity (MMN), P3a, and reorienting negativity (RON) were modulated by age and by voluntary attention. P3a was additionally affected by distractor strength. Maturational changes were also observed in the amplitudes of P1 (decreasing with age) and N1 (increasing with age). P2-modulation by voluntary attention was opposite in young children and adults. CONCLUSIONS: Results suggest quantitative and qualitative changes in auditory voluntary and involuntary attention and distraction during development. The processing steps involved in distraction (pre-attentive change detection, attention switch, reorienting) are functional in children aged 6-8 but reveal characteristic differences to those of young adults. In general, distractibility as indicated by behavioral and ERP measures decreases from childhood to adulthood. SIGNIFICANCE: Behavioral and ERP markers for different processing stages involved in voluntary and involuntary attention reveal characteristic developmental changes from childhood to young adulthood.     

Enhanced production of endothelium-derived contracting factor by endothelial cells subjected to pulsatile stretch

The purpose of this study was to assess the role of cyclic deformation in modulating the production by endothelial cells (ECs) in culture of a recently described endothelium-derived smooth muscle cell contracting factor, endothelin. We grew bovine aortic ECs to confluence on culture plates with flexible membrane bottoms. Vacuum (-20 kPa) was applied to deform the membrane to 24% strain at 60 cycles/min for 1, 3, or 5 days. Control ECs were grown on the same membrane but without vacuum deformation. The conditioned media were collected, centrifuged at 10,000 rpm for 10 minutes to remove cells and debris, and the supernatant fluid was subjected to radioimmunoassay for endothelin. The results demonstrate that bovine aortic ECs release a basal level of endothelin under stationary conditions (107.1 +/- 14.7 pg/10(5) cells), and this production increased fivefold to sixfold with cyclic stretch. Thus physical forces exerted on ECs in culture can influence the secretion of this vasoconstrictive molecule.     

华蟾蜍毒素对离体豚鼠输精管的作用

华蟾蜍毒素(华蟾素)使离体豚鼠输精管产生剂量依赖性收缩反应,利血平化豚鼠输精管及冷藏输精管对华蟾素反应减弱。给酚妥拉明、维拉帕米后,输精管对华蟾素反应均受抑制,溴苄胺可使反应潜伏期缩短。结果提示华蟾素收缩输精管反应可能与其促进肾上腺素能神经末稍NA释放有关。     

Perfluorochemicals as US contrast agents for tumor imaging and hepatosplenography: preliminary clinical results

In animals, perfluorochemicals (PFCs) are effective ultrasound (US) contrast agents that produce hepatic, splenic, and tumor enhancement. The use of Fluosol-DA 20%, an emulsion of perfluorodecalin and perfluorotripropylamine, was studied in nine non-critically ill patients with cancer who had liver lesions. US studies without Fluosol were compared with studies obtained 24, 48, and 72 hours after Fluosol infusion. Vital signs and extensive laboratory analyses are performed before and after Fluosol infusion. Liver metastases from colonic, pancreatic, and gastric carcinoma exhibited rim or diffuse enhancement after a Fluosol dose of 1.6 g/kg or greater. Fluosol produced echogenic enhancement of the liver and spleen relative to kidney at a dose of 2.4 g/kg, allowing the detection of nonenhancing lesions. In addition, Fluosol at a dose of 1.6 g/kg or greater allowed detection of lesions not seen before contrast medium was administered in three of the seven patients studied. There was a mild increase in the level of serum glutamic oxaloacetic transaminase in two patients, one given 2.4 and the other 3.2 g/kg of Fluosol. Mild and transient allergic reactions without change in vital signs were experienced by two patients.     

Reactivating potency of obidoxime, pralidoxime, HI 6 and HLö 7 in human erythrocyte acetylcholinesterase inhibited by highly toxic organophosphorus compounds

The treatment of poisoning by highly toxic organophosphorus compounds (nerve agents) is unsatisfactory. Until now, the efficacy of new potential antidotes has primarily been evaluated in animals. However, the extrapolation of these results to humans is hampered by species differences. Since oximes are believed to act primarily through reactivation of inhibited acetylcholinesterase (AChE) and erythrocyte AChE is regarded to be a good marker for the synaptic enzyme, the reactivating potency can be investigated with human erythro‐cyte AChE in vitro. The present study was undertaken to evaluate the ability of various oximes at concentrations therapeutically relevant in humans to reactivate human erythrocyte AChE inhibited by different nerve agents. Isolated human erythrocyte AChE was inhibited with soman, sarin, cyclosarin, tabun or VX for 30?min and reactivated in the absence of inhibitory activity over 5–60?min by obidoxime, pralidoxime, HI 6 or HLö 7 (10 and 30?μM). The AChE activity was determined photometrically. The reactivation of human AChE by oximes was dependent on the organophosphate used. After soman, sarin, cyclosarin, or VX the reactivating potency decreased in the order HLö 7 > HI 6 > obidoxime > pralidoxime. Obidoxime and pralidoxime were weak reactivators of cyclosarin-inhibited AChE. Only obidoxime and HLö 7 reactivated tabun-inhibited AChE partially (20%), while pralidoxime and HI 6 were almost ineffective (5%). Therefore, HLö 7 may serve as a broad-spectrum reactivator in nerve agent poisoning at doses therapeutically relevant in humans.     

Proliferation of endothelial cells in estrogen-stimulated rat liver. A light and electron microscopic cytochemical study.

The mononuclear phagocytes (Kupffer cells) in the normal rat liver can be distinguished from the endothelial cells on the basis of their endogenous peroxidase activity in the endoplasmic reticulum and their exclusive ability to phagocytose large (0.81 mum.) latex particles. Using these cellular markers we have investigated the effects of an estrogen upon the mitotic activity and the ultrastructure of individual types of littoral cells in the rat liver. Adult female rats received a single 10-mg. injection of diethylstilbestrol, and at daily intervals up to 6 days their livers were fixed by perfusion and processed for localization of peroxidase. Mitotic figures were rare in untreated control animals, but dividing littoral cells with both positive and negative peroxidase reaction could be identified. The exclusive localization of injected latex particles in dividing peroxidase-positive cells indicated that peroxidase reaction identified the Kupffer cells not only in the interphase but also during the mitotic division. In estrogen-treated animals there was a sharp rise in the mitotic activity of littoral cells; the activity reached its peak on the 3rd day and returned to normal levels on the 6th day after the initial injection. A breakdown of the dividing cells on the basis of their peroxidase reactivity revealed that nearly the entire population of dividing cells consisted of peroxidase-negative endothelial cells. In addition, numerous hyperactive Kupffer cells containing large phagolysosomes with phagocytosed peripheral blood cells and latex particles were seen. Intermediate cell-types with cytochemical features between Kupffer cells and endothelial cells or between monocytes and Kupffer cells were not encountered. Because of the limited phagocytic capacity of hepatic endothelial cells, our observations would provide morphologic evidence in support of previous physiologic studies, indicating that estrogen treatment has little or no effect upon the particle clearing function of the reticuloendothelial system in rats. The rare but clear demonstration of dividing Kupffer cells in liver sinusoids would indicate that these cells are capable of self-replication in situ. Finally, our observations suggest that estrogens may play an important role in the pathophysiology of endothelial cells.