Basis for phospholipid incorporation into peripheral nerve myelin

To characterize the mechanism(s) for targeting of phospholipids to peripheral nerve myelin, we examined the kinetics of incorporation of tritiated choline-, glycerol-, and ethanolamine-labeled phospholipids into four subfractions: microsomes, mitochondria, myelin-like material, and purified myelin at 1, 6, and 24 h after precursors were injected into sciatic nerves of 23-24-day-old rats. As validation of the fractionation scheme, a lag (> 1 h) in the accumulation of labeled phospholipids in the myelin-containing subfractions was found. This lag signifies the time between synthesis on organelles in Schwann cell cytoplasm and transport to myelin. In the present study, we find that sphingomyelin (choline-labeled) accumulated in myelin-rich subfractions only at 6 and 24 h, whereas phosphatidylserine (glycerol-labeled) and plasmalogen (ethanolamine-labeled) accumulated in the myelin-rich fractions by 1 h. The later phospholipids accumulate preferentially in the myelin-like fraction. These results are consistent with the notion that the targeting of sphingomyelin, a lipid present in the outer myelin leaflet, is different from the targeting of phosphatidylserine and ethanolamine plasmalogen, lipids in the inner leaflet. These findings are discussed in light of the possibility that sphingomyelin targeting is Golgi apparatus based, whereas phosphatidylserine and ethanolamine plasmalogen use a more direct transport system. Furthermore, the routes of phospholipid targeting mimic routes taken by myelin proteins P0 (Golgi) and myelin basic proteins (more direct).     

Dual-path capacitance compensation network for microelectrode recordings

Commercially available microelectrode preamplifiers have a built-in capacity compensation circuit. When a shielded cable is utilized to transmit the signal from the microelectrode to the preamplifier the compensative ability of this circuit may be inadequate and may result in a less than desired frequency response. We describe a dual-path capacitance compensation circuit that resolves this problem without impairment of the shielding properties.     

Single unit recording capabilities of a 100 microelectrode array

We have developed a three-dimensional silicon electrode array which provides 100 separate channels for neural recording in cortex. The device is manufactured using silicon micromachining techniques, and we have conducted acute recording experiments in cat striate cortex to evaluate the recording capabilities of the array. In a series of five acute experiments, 58.6% of the electrodes in the array were found to be capable of recording visually evoked responses. In the most recent acute study, the average signal-to-noise ratio for recordings obtained from 56 of the electrodes in the array was calculated to be 5.5:1. Using standard window discrimination techniques, an average of 3.4 separable spikes were identified for each of these electrodes. In order to compare the two-dimensional mapping capabilities of the array with those derived from other technologies, orientation preference and ocular dominance maps were generated for each of the evoked responses. Histological evaluation of the implant site indicates some localized tissue insult, but this is likely due to the perfusion procedure since high signal-to-noise ratio neural responses were recorded. The recording capabilities of the Utah Intracortical Electrode Array in combination with the large number of electrodes available for recording make the array a tool well suited for investigations into the parallel processing mechanisms in cortex.     

500kA铝电解槽改成600kA的设计

2000年,M．Dupuis,V．Bojarevis曾经直接将300kA电解槽的设计翻新改成350kA设计,继而又利用延长槽壳作了400kA的热一电场设计。2003年,作者又进一步加长和稍微加宽了槽壳,提出了500kA的热一电场设计。2005年之后,又将500kA槽壳继续加长提出一种740kA的热一电场设计,并声称从热一电场的热平衡设计来看电解槽的大小不受限制。最终在2005年6月,作者提出了500kA和740kA电解槽的MHD和槽壳的机械设计,从MHD和槽壳的机械性能方面分析似乎电解槽的大小也不受限制。最近新建的铝厂或大型电解槽实验工厂也都在使用更大电流的电解槽,例如在中国。由此可以确信,在近几年不断出现新技术和控制技术的支撑条件下,电解槽容量将继续增大。     

进风井石门巷两道三分法工程在三山岛金矿的应用

随着近地表资源的日益枯竭,矿山地下开采由浅部区域进入深部区域已成为发展趋势,通风系统的完善程度直接制约矿山向深部发展。针对三山岛金矿采掘作业面通风紊乱,通风环境恶化的问题,通过采用进风井石门巷两道三分法工程,建立风门、风窗对新鲜风流合理疏导、调节,达到定向、定量输送新鲜风通往深部的目的。该工程的应用不仅保证了现有生产、掘进的需风量,同时增加了深部进风量,并通过风门、封闭墙实现人车分流、调控分风等功能,具有一定的先进性,可为同类型矿山提供借鉴。     

Pyramidal nerve cell loss in Alzheimer''s disease

Despite clinical evidence from the National Institutes of Health consensus panel in 1991 that breast-conservation surgery (BCS) with radiation therapy (RT) is appropriate treatment in early-stage breast cancer, the overall rate of acceptance and actual practice of BCS with RT has remained low. We retrospectively reviewed 228 cases of breast cancer in female patients with stage Tis, I or II breast cancer treated between 1987 and 1995. Thirty-five cases (15.4%) were stage Tis, 70 cases (30.7%) were stage I, and 123 cases (53.9%) were stage II, Overall, 57% of Tis, I or II breast cancers received conservative treatment; 57% of stage Tis, 79% of stage I, and 44% of stage II tumors. These rates of conservative therapy are higher than in other reported series in the literature. BCS with RT produces equivalent rates of morbidity and survival as MRM, and, because it preserves the breast, is preferable for the majority of women who present with stage Tis, I, or II breast cancer.     

Filamentous nerve cell inclusions in neurodegenerative diseases

Recent work has shown that abnormal filamentous inclusions within some nerve cells is a characteristic shared by Alzheimer's disease, some frontotemporal dementias, Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, as well as Huntington's disease and other trinucleotide repeat disorders. This suggests that in each of these disorders, the affected nerve cells degenerate as a result of these abnormal inclusions. Except for trinucleotide repeat disorders, the filaments involved have been shown to consist of either the microtubule-associated protein tau or alpha-synuclein. Over the past year, mutations in the genes for tau and alpha-synuclein have been identified as the genetic causes of some familial forms of frontotemporal dementia and Parkinson's disease, respectively. The discovery last year of neuronal intranuclear inclusions in Huntington's disease and other disorders with expanded glutamine repeats has suggested a unifying mechanism underlying the pathogenesis of this class of neurodegenerative diseases.     

锆-茜素红络合物在碳黑微电极上的阳极吸附伏安法研究

通过研究锆-茜素红络合物在碳黑微电极上的阳极吸附伏安行为,提出了一种测定痕量锆的新方法。在极谱分析仪上采用二次导数线性扫描伏安法进行分析,在0.128 mol/L氨基乙酸-0.048 mol/L邻苯二甲酸氢钾缓冲溶液(pH 4.3)中,在200 mV富集60 s,从200~1 200 mV以200 mV/s的速率线性扫描,研究发现,络合物吸附在碳黑微电极表面,于860 mV(vs.SCE)处产生一灵敏的溶出峰,为络合物中配体茜素红的氧化所产生。峰电流与锆的浓度在6.0×10-11~2.0×10-7mol/     

A new mutagenicity assay method for frameshift mutagens based on deleting or inserting a guanosine nucleotide in the beta-lactamase gene

The conventional method of site-directed mutagenesis was used to develop two Salmonella strains, JK-1 and JK-2, for detecting frameshift mutagens. The JK-1 strain was derived from Salmonella typhimurium TA1537 strain transformed by a mutant construct. A guanosine nucleotide was inserted between nucleotide residues 312 and 313 of the beta-lactamase gene. The JK-2 strain was obtained by the same procedure, but a guanosine nucleotide in position 315 of the beta-lactamase gene was deleted. The strains were tested with ten frameshift mutagens and the revertants were selected by ampicillin resistance. Representative mutagens including 2-nitrofluorene (2-NF), 2-acetylaminofluorene (AAF), 9-aminoacridine (9-AA), 2,7-diaminofluorene (2,7-DAF) and 2-methoxy-6-chloro-9-(3-(ethyl-2-chloro-ethyl)-aminopropylamino)acridine (ICR-170) were more potent in the JK-1 strain than the JK-2 strain, and the number of revertant colonies were dose related. Under the same conditions, the ampicillin test was more sensitive than the Ames test. Other types of compounds such as 2-methoxy-6-chloro-9-(2-chloroethylaminopropylamino)acridine (ICR-191), benzo[a]pyrene (BP), 4-nitroquinoline N-oxide (4-NQNO), hycanthone and aflatoxin B1 (AFB1) were not as mutagenic to these new strains. The method is quite promising for studying certain specific frameshift mutagens, but more chemical mutagens should be tested to validate its applicability and reproducibility in general use.     

Phosphatidylcholine-specific phospholipase C regulates glutamate-induced nerve cell death

Phosphatidylcholine-specific phospholipase C (PC-PLC) is a necessary intermediate in transducing apoptotic signals for tumor necrosis factor and Fas/Apo-1 ligands in nonneuronal cells. The data presented here show that PC-PLC also is required in oxidative glutamate-induced programmed cell death of both immature cortical neurons and a hippocampal nerve cell line, HT22. In oxidative glutamate toxicity, which is distinct from excitotoxicity, glutamate interferes with cystine uptake by blocking the cystine/glutamate antiporter, indirectly causing a depletion of intracellular glutathione. A PC-PLC inhibitor blocks oxidative glutamate toxicity, and exogenous PC-PLC potentiates glutamate toxicity. The inhibition of PC-PLC uncouples the cystine uptake from glutamate inhibition, allowing the maintenance of glutathione synthesis and cell viability. These data suggest that PC-PLC modulates neuronal cell death through a mechanism that is distinct from that involved in nonneuronal apoptosis.