希捷Pharaoh系列硬盘 低温启动异常解决办法

故障现象:希捷硬盘在温度较低的环境(0～10度)下,第一次冷开机时可能存在启动时间长(例如在WINDOWS滚动条处长时间滚动)、硬盘异响、检测不到硬盘或进入系统后运行速度非常慢的情况,如果重     

按部就班 富勒U79无线套装对码方法

富勒U79无线套装更换新的接收器后发现无法使用,拨打400免费服务热线后了解到,无线键鼠即使是更换同一型号的接收器也需要重新对码才能再次使用。由于这套键鼠宣传时提示采用了智能自动对码技术,可即插即用,因而不少用户出现键鼠无法使用时都会对如何进行对码操作产生疑问,特别     

用手指打高尔夫 Great Wall Z2588 touch体验

打高尔夫球是一项具有特殊魅力的运动,人们在天然优雅的自然的绿色环境中锻炼身体、陶冶情操,更可彰显个人高贵优雅的气质。而今天,Great Wall将高尔夫运动概念与桌面显示器融合在一起,推出支持多点触控操作的Z2588 touch,让用户动动手指即可"潇洒挥杆"——     

Reduction of disulfide bonds in an amyloidogenic Bence Jones protein leads to formation of "amyloid-like" fibrils in vitro

Motivated by the finding that the amino acid sequence of the Bence Jones protein BJP-DIA was identical to that of the main protein component of the amyloid fibrils obtained from the same patient with AL-amyloidosis, (Klafki, H.-W., Kratzin, H.-D., Pick, A.-I., Eckart, K., Karas, M. & Hilschmann, N. (1992) Biochemistry 31, 3265-3272.), we attempted to create "amyloid-like" fibrils from the Bence Jones protein in vitro, without addition of proteolytic enzymes. Reduction of BJP-DIA, solubilized in PBS, pH 7.4, overnight at 37 degrees C resulted in the formation of a precipitate which had affinity for the dye Congo red. Electron microscopy of negatively stained samples of the reduced protein revealed aggregates of linear unbranched fibrils. SDS-polyacrylamide gel electrophoresis demonstrated that the precipitate consisted almost exclusively of intact light chain molecules. This result makes it possible to deduce a molecular model of these amyloid fibrils generated in vitro.     

Treatment of schizophrenic psychoses with Lyorodin

Forty-four patients suffering from acute and chronic schizophrenic psychoses were used to obtain, by using Lorr's scale (IMPS) and taking the changes in disease state observed within three months as a base, suggestions or pointers as to the proper treatment of disease with fluphenazine (lyorodin) which is a neuroleptically highly potent phenothiazine derivative. Megalomania, grandiose delusions apathetic and depressive syndromes showed marked tendencies toward major improvement. An "antiautistic" effect was observed in chronic patients. The effective dose was between 6 and 12 mg a day. The drug was well tolerated. In the majority of cases it was also necessary for antiparkinsonian drugs to be administered to patients. After twelve months of treatment, slight to major improvements or even freedom from symptoms could be observed in 28 cases (or 64%).     

Molecular genetics of rust resistance in poplars (Melampsora larici-populina Kleb/Populus sp.) by bulked segregant analysis in a 2 x 2 factorial mating design

With random amplified polymorphic DNA (RAPD) markers, we have tagged a genomic region in Populus sp. involved in qualitative resistance to Melampsora larici-populina. Our approach was based on three steps: use of RAPD markers that can be quickly and efficiently researched: application of "bulked segregant analysis" technique on individuals of one interspecific family P. trichocarpa x P. deltoides to search for RAPD markers linked to resistance; and validation of these markers in two other families linked with the first one in a 2 x 2 factorial mating design. Of five detected markers, only one marker M03/04_480 was polymorphic in the three segregating families, involving 89 individuals and four different parents. We have estimated the recombination value of 1 cM with 1 cM sampling error.     

Evaluation of nefazodone as a serotonin uptake inhibitor and a serotonin antagonist in vivo

Nefazodone (2-[3-[4-(3-chlorophenyl)-1-piperazinyl]propyl]-5-ethyl- 2,4-dihydro-4-(2-phenoxyethyl)-3H-1,2,4-triazol-3-one) has been reported to be effective in the treatment of depression. Antagonism of serotonin type 2A (5HT2A) receptors, as well as inhibition of the serotonin (5HT) uptake carrier, has been suggested to contribute to the antidepressant action of nefazodone in vivo (Eison et al., 1990). Nefazodone weakly antagonized the quipazine-induced rise in rat serum corticosterone levels and the quipazine-induced increase in rat hypothalamic 3-methoxy-4-hydroxy-phenylglycol sulfate, suggesting blockade of 5HT2A receptors in vivo. Nefazodone, however, failed to antagonize the p-chloroamphetamine-induced depletion of mouse or rat brain 5HT, displaying a lack of effect on the 5HT uptake carrier. These data extend previous in vitro and in vivo data (Eison, et al. 1990) reporting nefazodone to be an antagonist at 5HT2A receptors, but fail to show inhibition of the 5HT uptake carrier in the same dose range.     

Maturation of peroxisomes in differentiating human hepatoblastoma cells (HepG2): possible involvement of the peroxisome proliferator-activated receptor alpha (PPAR alpha)

Although several variant alleles at the human NAT1 gene locus have been reported, their relationship to phenotypic variations in NAT1 function remains unclear. We have used in-vivo and invitro phenotyping tests, along with PCR-based cloning and heterologous expression, to investigate the extent of variation in NAT1 function and to characterize novel allelic variants at the NAT1 gene locus. The NAT1-selective substrate p-aminosalicylic acid (PAS) was used as a probe for NAT1 function. In-vivo PAS acetylation rates were estimated by determining the ratio of PAS to N-acetylated PAS (AcPAS) in urine and plasma following the oral ingestion of Nemasol Sodium. Excluding outliers, a 65-fold variation in the urinary AcPAS:PAS ratio was observed (n = 144), while a 5.6-fold variation in the plasma AcPAS:PAS ratio was seen in a subset (n = 19) of this sample. Urinary and plasma ratios correlated moderately (r = 0.74, p < 0.0005). One individual (case 244) had a marked impairment of PAS N-acetylation, with 10-fold lower urinary and plasma AcPAS:PAS ratios compared with other subjects. Biochemical investigations in whole blood lysates from case 244 suggested a NAT1 kinetic defect, with a 20-fold increased apparent K(m) for PAS and a 90-fold decreased Vmax for AcPAS formation. We subcloned, sequenced and expressed the protein-coding regions of the NAT1 alleles from case 244 and from seven other selected probands. Sequence analysis revealed the presence of two new variant alleles, designated as NAT1 x 14 and NAT1 x 15, in case 244, as well as one variant, NAT1 x 11, which has been observed in previous investigations. NAT1 x 14 contained a missense mutation (G560-->A) that is predicted to change a single amino acid (Arg187-->Gln), as well as two 3' non-coding region mutations (T1088-->A and C1095-->A) that have previously been observed in the NAT1 x 10 allelic variant. NAT1 x 15 had a single nonsense mutation (C559-->T; Arg187-->stop) and, thus, encodes a truncated protein. The activity of recombinant NAT1 14 mirrored the defective enzyme function in whole blood lysates from case 244, while NAT1 15 was completely inactive. Expressed NAT1 11, on the other hand, had identical activity to the wild type NAT1 4 allele, suggesting that the coding region mutations in this variant are functionally silent. The frequencies of NAT1 x 11, NAT1 x 14 and NAT1 x 15 were 0.021, 0.028 and 0.014 (n = 288 alleles), respectively, suggesting that they are relatively rare in our predominantly Caucasian sample.     

A computer-controlled spraying-freezing apparatus for millisecond time-resolution electron cryomicroscopy

The application of gene therapy techniques to the clinical problem of coronary restenosis has generated tremendous attention and enthusiasm. Use of gene transfer technology to prevent a common intractable illness would represent a watershed event for human gene therapy. However, the time is not yet right to initiate gene therapy trials for restenosis. The biology of restenosis is incompletely understood, catheter-based gene delivery is poorly adapted to the coronary circulation, and current gene transfer vectors are ill-suited for safe and effective gene delivery to the coronary artery wall. Basic research designed to overcome these obstacles is currently more appropriate than the initiation of clinical trials.