基于多重绘制模型的艺术绘制

为了使得计算机能自动生成表达力丰富的三维场景的艺术绘制，提出了一种基于Shader的多重绘制模型，并采用了多重绘制的协调、参数空间的纹理铺陈、基于色调的表现控制等技术来进行模拟．引入多重绘制可以同时采用对象空间的绘制和图像空间的绘制，通过纹理铺陈描述语言Shader，用户可以定义自己的纹理和笔划来表现三维和二维场景．不同于传统的Shader，基于Shader的多重绘制模型采用光亮度、材质颜色等作为输入，由用户自行决定绘制结果的输入．这一用户可定制性的引入大大增强了艺术绘制的表现能力．该模型已经在一个建筑设计系统中得到实现，以钢笔画为表现媒介的图例表明该模型模拟效果令人满意．     

Reactive sputter etching of Al in BCl3

Etching of Al is studied in pure BCl₃ as well as in mixtures with other gases in the reactive sputter etching mode in a cryopumped system. Etch rate, selectivity with respect to positive photoresist, SiO₂ and Si and etch profiles are investigated as a function of gas composition, gas pressure, flow rate and plasma power. Plasma chemical processes are monitored by quadrupole mass spectroscopy as well as by optical emission spectroscopy. Perfectly square Al-profiles can be etched if etch rates are kept below 1000 A/min. Al-patterns running over steep steps can also be clearly defined if a certain amount of overetching can be tolerated. The experimental data indicate that the etch process is reactant supply limited. Anisotropic etching is achieved by either a ‘surface inhibitor mechanism’ or the formation of a sidewall protecting film.     

一种通用的trimmed曲面三角化算法

本文提出一种既可用于进行trimmed曲面求交,也可用于进行trimmed曲面显示的快速trimmed曲面三角化算法。算法主要基于本文首次提出的对trimmed曲面的空间及参数trimmed边界进行相关离散的思想和入边、出边、跨边三角形等新概念。算法已经成功地应用于雕塑立体造型系统MESSAGE中,进行trimmed曲面的求交与显示。     

K+] dependence of open-channel conductance in cloned inward rectifier potassium channels (IRK1, Kir2.1)

Potassium conduction through unblocked inwardly rectifying (IRK1, Kir2.1) potassium channels was measured in inside-out-patches from Xenopus oocytes, after removal of polyamine-induced strong inward rectification. Unblocked IRK1 channel current-voltage (I-V) relations show very mild inward rectification in symmetrical solutions, are linearized in nonsymmetrical solutions that bring the K+ reversal potential to extreme negative values, and follow Goldman-Hodgkin-Katz constant field equation at extreme positive E alpha. When intracellular K+ concentration (KIN) was varied, at constant extracellular K+ concentration (KOUT) the conductance at the reversal potential (GREV) followed closely the predictions of the Goldman-Hodgkin-Katz constant field equation at low concentrations and saturated sharply at concentrations of > 150 mM. Similarly, when KOUT was varied, at constant KIN, GREV saturated at concentrations of > 150 mM. A square-root dependence of conductance on KOUT is a well-known property of inward rectifier potassium channels and is a property of the open channel. A nonsymmetrical two-site three-barrier model can qualitatively explain both the I-V relations and the [K+] dependence of conductance of open IRK1 (Kir2.1) channels.     

Ophthalmic findings with partial trisomy (duplication) of the long arm of chromosome 7

BACKGROUND: The sensitivity of diagnostic imaging of processes in the parotid gland has been increased by improved spatial resolution, yet specificity remains unchanged. The purpose of this study was to determine whether the low-flow color duplex technique alters the specificity of B-mode ultrasonography. PATIENTS AND METHODS: Forty-one patients with tumors of the parotid gland were examined by color duplex echography as well as histologically. Twenty-eight of the 41 patients had benign tumors and 13 had malignant disease. In 17 of 41 patients, color duplex ultrasonography failed to detect any vascularization within the tumor. Histopathological examination showed that 3 of these 17 tumors were malignant and 14 of 17 were benign. Intranodal vascularization was detected in 24 cases. Ten of these patients were found to have malignant tumors of the parotid gland; 14 had benign parotid tumors. RESULTS: Our present findings show that marked intratumoral vascularization especially appears in malignant tumors. In contrast to lymph nodes, the location and texture of intranodal blood vessels do not provide information about the nature of the neoplasm. CONCLUSIONS: Low flow duplex ultrasonography does not increase the specificity of preoperative examination in tumors of the parotid gland.     

Leptin attenuates respiratory complications associated with the obese phenotype

A profile of respiratory complications has been associated with the onset and development of obesity in humans. Similar phenotypes have been routinely demonstrated in genetic animal models of obesity such as the ob mouse (C57BL/6J-Lepob). The objective of the present study was to test the hypothesis that a constellation of respiratory complications are attenuated with leptin (i.e., protein product of the ob gene) replacement. Daily leptin administration during a 6-wk period was conducted to control body weight of mutant ob mice similar to genotypic control groups. During the treatment period, repeated baseline ventilatory measurements were assessed by using whole body plethysmography while quasistatic pressure-volume curves were performed to further explore the role of leptin in improving lung mechanics. Diaphragmatic myosin heavy chain (MHC) isoform phenotype was examined to determine proportional changes in MHC composition. In room air, breathing frequency and minute ventilation were significantly (P < 0.01) different among ob treatment groups, suggesting that leptin opposed the development of a rapid breathing pattern observed in vehicle-treated ob mice. Quasistatic deflation curves indicated that the lung volume of leptin-treated ob mice was significantly (P < 0.05) greater relative to vehicle-treated ob mice at airway pressures between 0 and 30 cmH2O. Diaphragm MHC composition of leptin-treated ob mice was restored significantly (P < 0.05) to resemble the control phenotype. In this genetic mouse model of obesity, the results suggested that respiratory complications associated with the obese phenotype, including rapid breathing pattern at baseline, diminished lung compliance, and abnormal respiratory muscle adaptations, are attenuated with prolonged leptin treatment.     

Interactions of GYKI 52466 and NBQX with cyclothiazide at AMPA receptors: experiments with outside-out patches and EPSCs in hippocampal neurones

In outside-out patches from cultured hippocampal neurones, glutamate (1 mM) applied for 1 ms evoked currents which rose rapidly (tau(on) 451 +/- 31 micros) to a peak and then deactivated with slower kinetics (1.95 +/- 0.13 ms). Offset time constants were significantly slower with longer application durations (tau(off) 3.10 +/- 0.19, 3.82 +/- 0.25, 4.80 +/- 0.65 and 7.56 +/- 0.65 ms with 10, 20, 100 and 500 ms applications respectively). Desensitization was complete within 100 ms with a similar rate for all application durations (4.74 +/- 0.34 ms with 100 ms applications). GYKI 52466 reduced inward peak currents with an IC50 of 11.7 +/- 0.6 microM and had similar potency on steady-state currents to longer glutamate applications. GYKI 52466 had no significant effect on desensitization or deactivation time constants but caused a modest and significant prolongation of onset kinetics at higher concentrations. Cyclothiazide (100 microM) potentiated steady-state currents 25-fold at 100 ms and caused a modest but significant slowing in onset kinetics (601 +/- 49 micros with 1 ms applications) but a more pronounced prolongation of deactivation time constants (5.55 +/- 0.66 ms with 1 ms applications). In 50% of neuronal patches cyclothiazide completely eliminated desensitization. In those patches with residual desensitization, the rate was not significantly different to control (5.36 +/- 0.43 ms with 100 ms applications). Following 100 ms applications of glutamate, GYKI 52466 had IC50s of 11.7 +/- 1.1 microM and 75.1 +/- 7.0 microM in the absence and presence of cyclothiazide (100 microM) respectively. Onset kinetics were slowed from 400 +/- 20 micros to 490 +/- 30 micros by cyclothiazide (100 microM) and then further prolonged by GYKI 52466 (100 microM) to a double exponential function (tau(on1) 1.12 +/- 0.13 ms and tau(on2) 171.5 +/- 36.5 ms). GYKI 52466 did not re-introduce desensitization but concentration-dependently weakened cyclothiazide's prolongation of deactivation time constants (1 ms applications: 5.01 +/- 0.71, 4.47 +/- 0.80 and 2.28 +/- 0.64 ms with GYKI 52466 30, 100 and 300 microM respectively). NBQX reduced peak current responses with an IC50 of 28.2 +/- 1.3 nM. Paradoxically, steady-state currents with 500 ms applications of glutamate were potentiated from 3.3 +/- 1.2 pA to 29.4 +/- 6.4 pA by NBQX (1 nM). Higher concentrations of NBQX then antagonized this potentiated response. The potency of NBQX in antagonizing steady-state currents to 500 ms applications of glutamate (IC50 120.9 +/- 30.2 nM) was 2-fold less than following 100 ms applications (IC50 67.7 +/- 2.6 nM). NBQX had no effect on rapid onset, desensitization or deactivation time constants. However, a slow relaxation of inhibition was seen with longer applications. NBQX was 2-5-fold less potent against inward currents in the presence of cyclothiazide (100 microM) depending on the application duration but had no effect on the rapid onset, desensitization or deactivation time constants. The same relaxation of inhibition was seen as with NBQX alone. NBQX (1 microM) reduced AMPA receptor-mediated EPSC amplitude to 7 +/- 1% of control with no effect on kinetics. Cyclothiazide (330 microM) caused a 2.8-fold prolongation of the decay time constant (control 26.6 +/- 2.2 ms, cyclothiazide 74.2 +/- 7.6 ms, n = 9). Additional application of NBQX (1 microM) partly reversed this prolongation to 1.9 fold (47.7 +/- 2.5 ms, n = 5). These results support previous findings that cyclothiazide also allosterically influences AMPA receptor agonist/antagonist recognition sites. There were no interactions between NBQX and cyclothiazide on desensitization or deactivation time constants of glutamate-induced currents but clear interactions on EPSC deactivation kinetics. This raises the possibility that the interactions of NBQX, GYKI 52466 and cyclothiazide on AMPA-receptor-mediated EPSC kinetics observed are due to modulation of glutamate-release at presynaptic AMPA receptors.     

Anagrelide in control of myeloproliferative thrombocythemia: long-term experiences in 6 patients

Symptomatic or asymptomatic chronic elevation of platelet count can be observed in all forms of myeloproliferative disorders (MPD). Benefits and limitations of the traditional platelet-reducing agents, such as radioactive phosphorus, alkylating agents, hydroxyurea and interferon alpha, are well known and have been largely described. Anagrelide (Agrelin) is an additional newer drug with a selective platelet-lowering effect. We describe our own long-term experience in 6 patients with MPD who were treated with anagrelide as part of a compassionate-use protocol between April 1991 and August 1997. The median duration of therapy was 54 months (range 17 to 75 months), with an overall response rate of 100% (complete and partial response for at least 4 weeks). The initial median platelet count of 1211 x 10(9)/l (range 847 to 2050 x 10(9)/l) was reduced rapidly and lastingly to 570 x 10(9)/l (range 216 to 667 x 10(9)/l) at the time of the last control. Under treatment with anagrelide 4 of the 6 patients showed a reduction of disease-associated symptoms or complications. Adverse reactions were generally mild and transitory, and no interruption or cessation of therapy was required. Development of drug resistance or late adverse events were not observed. Treatment with anagrelide is effective, safe and in our opinion easy to administer. It also appears to be suitable for long-term administration.