沉积温度对热舟蒸发MgF2薄膜性能的影响

采用热舟蒸发方法沉积了氟化镁（MgF2）材料的单层膜，沉积温度从200℃上升到350℃，间隔为50℃。测量了样品的透射率和反射率光谱曲线，进行了表面粗糙度的标定，并在此基础上进行了光学损耗及散射损耗的计算。同时对355nm波长处的激光诱导损伤阈值进行了测量。结果表明：随着沉积温度的升高，光学损耗增加;在短波长范围散射损耗在光学损耗中所占比例很小，光学损耗的增加主要由吸收损耗引起；在355nm波长处的损伤阈值变化与吸收损耗的变化趋势相关，损伤机制主要是吸收起主导作用。样品的微缺陷密度也是影响损伤阈值的一个重要因素，损伤阈值随缺陷密度的增加而降低。

热舟蒸发LaF_3薄膜的紫外性能研究

研究了沉积温度对热舟蒸发氟化镧薄膜结构和光学性能的影响,沉积温度从200℃上升到350℃,间隔为50℃.采用分光光度计测量了样品的透射率和反射率光谱曲线,并在此基础上进行了光学损耗、光学常数以及带隙和截止波长的计算.采用表面轮廓仪进行了表面形貌和表面粗糙度的标定,采用X射线衍射(XRD)方法测量了不同沉积温度下样品的微结构.发现在短波长波段,随着沉积温度的升高,光学损耗增加,晶粒尺寸增大,表面粗糙度略有增加.不过散射损耗在光学损耗中所占比例均很小,光学损耗的增加主要由吸收损耗引起.随着沉积温度的升高,折射率与消光系数增大,带隙变小,相对应的截止波长向长波方向移动.

355nm增透膜的设计、制备与性能

用热舟蒸发法结合修正挡板技术制备了355 nm LaF3/MgF2增透膜,并对部分样品进行了真空退火。采用Lambda 900光谱仪测试了增透膜的低反光谱和透射光谱,并考察了其光谱稳定性;使用脉冲8 ns的355 nm激光测试了增透膜的激光损伤阈值(LIDT);采用Normarski显微镜对增透膜的表面缺陷密度和破斑形貌进行了观察。实验结果表明,制备得到的增透膜的剩余反射率较低,光谱稳定性好;真空退火对增透膜的激光损伤阈值没有改善;增透膜的破环形貌为散点形式,结合破斑深度测试表明薄膜的破坏源于薄膜和基底界面的缺陷点。JGS1熔石英基底由于有好的表面状况、固有的高激光损伤阈值和以其为基底的增透膜具有更低的表面场强,使得其上的增透膜有更高的抗激光损伤能力。

Molecular systematics of pikas (genus Ochotona) inferred from mitochondrial DNA sequences

The phylogenetic relationships among worldwide species of genus Ochotona were investigated by sequencing mitochondrial cytochrome b and ND4 genes. Parsimony and neighbor-joining analyses of the sequence data yielded congruent results that strongly indicated three major clusters: the shrub-steppe group, the northern group, and the mountain group. The subgeneric classification of Ochotona species needs to be revised because each of the two subgenera in the present classification contains species from the mountain group. To solve this taxonomic problem so that each taxon is monophyletic, i.e., represents a natural clade, Ochotona could be divided into three subgenera, one for the shrub-steppe species, a second for the northern species, and a third for the mountain species. The inferred tree suggests that the differentiation of this genus in the Palearctic Region was closely related to the gradual uplifting of the Tibet (Qinghai-Xizang) Plateau, as hypothesized previously, and that vicariance might have played a major role in the differentiation of this genus on the Plateau, On the other hand, the North American species, O. princeps, is most likely a dispersal event, which might have happened during the Pliocene through the opening of the Bering Strait. The phylogenetic relationships within the shrub-steppe group are worth noting in that instead of a monophyletic shrub-dwelling group, shrub dwellers and steppe dwellers are intermingled with each other. Moreover, the sequence divergence within the sister tars of one steppe? dweller and one shrub dweller is very low. These findings support the hypothesis that pikes have entered the steppe environment several times and that morphological similarities within steppe dwellers were due to convergent evolution. (C) 2000 Academic Press.

Origin of rabbit (Oryctolagus cuniculus) in China: evidence from mitochondrial DNA control region sequence analysis

A fragment of mitochondrial DNA (mtDNA) control region (similar to700 bp) was sequenced in 104 individuals from 20 breeds (three Chinese domestic breeds, five recently derived breeds and 12 introduced breeds) of domestic rabbits, Oryctolagus cuniculus . Nineteen sites were polymorphic, with 18 transitions and one insertion/deletion, and eight haplotypes (A1, A2, A3, A4, A5, A6, A7 and A8) were identified. Haplotype A1 was the most common and occurred in 89 individuals. In the 25 Chinese rabbits, only haplotype A1 was observed, while four haplotypes (A1, A3, A5 and A6) were found in 26 recently derived individuals. Haplotype A2 was shared by seven individuals among three introduced strains. The other six haplotypes accounted for 0. 96-1. 92% of the animals. Combined with the published sequences of European rabbits, a reduced median-joining network was constructed. The Chinese rabbit mtDNAs were scattered into two clusters of European rabbits. These results suggest that the (so-called) Chinese rabbits were introduced from Europe. Genetic diversity in Chinese rabbits was very low.

Molecular characterization of six Chinese families with m.3460G > A and Leber hereditary optic neuropathy

The primary mutation m.3460G > A occurs with a very low frequency (similar to 1%) in Chinese patients with Leber hereditary optic neuropathy (LHON). Up to now, there is no comprehensive study of Chinese patients harboring this mutation. We characterized six unrelated probands with m.3460G > A in this study, which were identified from 1,626 patients with LHON or suspected with LHON. The overall penetrance of LHON (25.6% [10/39]) in four pedigrees with m.3460G > A was substantially lower than those families with m.11778G > A (33.3% [619/1859]) as reported in our previous study. Intriguingly, family Le688 with a heteroplasmic m.3460G > A presented a lower penetrance (12.5%) than the other three families with a homoplasmic mutation. There is an elevated gender bias (affected male to affected female = 4:1) in the four families with m.3460G > A compared to those LHON families with m.11778G > A (2.4:1). Complete mtDNA sequencing indicated that the six matrilines belonged to haplogroups B4d1, F2, A5b, M12a, D4b2b, and D4b2, respectively. We did not identify any potential secondary mutation(s) that will affect or be associated with the penetrance of LHON in the six probands by using an evolutionary analysis and protein secondary-structure prediction. Taken together, our results suggested that the m.3460G > A mutation occurred multiple times in Chinese LHON patients. The heteroplasmic status of mutation m.3460G > A might influence the penetrance of LHON in family Le688.

Recombination Yet Inefficient Selection along the Drosophila melanogaster Subgroup's Fourth Chromosome

A central goal of evolutionary genetics is an understanding of the forces responsible for the observed variation, both within and between species. Theoretical and empirical work have demonstrated that genetic recombination contributes to this variation by breaking down linkage between nucleotide sites, thus allowing them to behave independently and for selective forces to act efficiently on them. The Drosophila fourth chromosome, which is believed to experience no-or very low-rates of recombination has been an important model for investigating these effects. Despite previous efforts, central questions regarding the extent of recombination and the predominant modes of selection acting on it remain open. In order to more comprehensively test hypotheses regarding recombination and its potential influence on selection along the fourth chromosome, we have resequenced regions from most of its genes from Drosophila melanogaster, D. simulans, and D. yakuba. These data, along with available outgroup sequence, demonstrate that recombination is low but significantly greater than zero for the three species. Despite there being recombination, there is strong evidence that its frequency is low enough to have rendered selection relatively inefficient. The signatures of relaxed constraint can be detected at both the level of polymorphism and divergence.

HSPC117 deficiency in cloned embryos causes placental abnormality and fetal death

Somatic cell nuclear transfer (SCNT) has been successfully used in many species to produce live cloned offspring, albeit with low efficiency. The low frequency of successful development has usually been ascribed to incomplete or inappropriate reprogramming of the transferred nuclear genome. Elucidating the genetic differences between normal fertilized and cloned embryos is key to understand the low efficiency of SCNT. Here, we show that expression of HSPC117, which encodes a hypothetical protein of unknown function, was absent or very low in cloned mouse blastocysts. To investigate the role of HSPC117 in embryo development, we knocked-down this gene in normal fertilized embryos using RNA interference. We assessed the post-implantation survival of HSPC117 knock-down embryos at 3 stages: E9 (prior to placenta formation); E12 (after the placenta was fully functional) and E19 (post-natal). Our results show that, although siRNA-treated in vivo fertilized/produced (IVP) embryos could develop to the blastocyst stage and implanted without any difference from control embryos, the knock-down embryos showed substantial fetal death, accompanied by placental blood clotting, at E12. Furthermore, comparison of HSPC117 expression in placentas of nuclear transfer (NT), intracytoplasmic sperm injection (ICSI) and IVP embryos confirmed that HSPC117 deficiency correlates well with failures in embryo development: all NT embryos with a fetus, as well as IVP and ICSI embryos, had normal placental HSPC117 expression while those NT embryos showing reduced or no expression of HSPC117 failed to form a fetus. In conclusion, we show that HSPC117 is an important gene for post-implantation development of embryos, and that HSPC117 deficiency leads to fetal abnormalities after implantation, especially following placental formation. We suggest that defects in HSPC117 expression may be an important contributing factor to loss of cloned NT embryos in vivo. (C) 2010 Elsevier Inc. All rights reserved.

Phylogenetic positions of several amitochondriate protozoa - Evidence from phylogenetic analysis of DNA topoisomerase II

Several groups of parasitic protozoa, as represented by Giardia, Trichomonas, Entamoeba and Microsporida, were once widely considered to be the most primitive extant eukaryotic group - Archezoa. The main evidence for this is their 'lacking mitochondria' and possessing some other primitive features between prokaryotes and eukaryotes, and being basal to all eukaryotes with mitochondria in phylogenies inferred from many molecules. Some authors even proposed that these organisms diverged before the endosymbiotic origin of mitochondria within eukaryotes. This view was once considered to be very significant to the study of origin and evolution of eukaryotic cells (eukaryotes). However, in recent years this has been challenged by accumulating evidence from new studies. Here the sequences of DNA topoisomerase 11 in G lamblia, T vaginalis and E histolytica were identified first by PCR and sequencing, then combining with the sequence data of the microsporidia Encephalitozoon cunicul and other eukaryotic groups of different evolutionary positions from GenBank, phylogenetic trees were constructed by various methods to investigate the evolutionary positions of these amitochondriate protozoa. Our results showed that since the characteristics of DNA topoisomerase 11 make it avoid the defect of 'long-branch attraction' appearing in the previous phylogenetic analyses, our trees can not only reflect effectively the relationship of different major eukaryotic groups, which is widely accepted, but also reveal phylogenetic positions for these amitochondriate protozoa, which is different from the previous phylogenetic trees. They are not the earliest-branching eukaryotes, but diverged after some mitochondriate organisms such as kinetoplastids and mycetozoan; they are not a united group but occupy different phylogenetic positions. Combining with the recent cytological findings of mitochondria-like organelles in them, we think that though some of them (e.g. diplomonads, as represented by Giardia) may occupy a very low evolutionary position, generally these organisms are not as extremely primitive as was thought before; they should be polyphyletic groups diverging after the endosymbiotic origin of mitochondrion to adapt themselves to anaerobic parasitic life.

POSTSYNAPTIC ALPHA-2 RECEPTOR STIMULATION IMPROVES MEMORY IN AGED MONKEYS - INDIRECT EFFECTS OF YOHIMBINE VERSUS DIRECT EFFECTS OF CLONIDINE

Very low doses (0.00001 mg/kg) of the alpha-2 adrenergic antagonist, yohimbine, improved working memory performance in a subset of aged monkeys. Improvement appeared to result from increased norepinephrine (NE) release onto postsynaptic alpha-2 adrenoceptors, as the response was blocked by the ''postsynaptic'' alpha-2 antagonist, SKF104078. Cognitive-enhancing effects of low dose yohimbine treatment may depend on aged animals retaining an intact, endogenous NE system. In contrast to yohimbine, the alpha-2 agonist, clonidine, has improved working memory in air aged animals examined. In the present study, clonidine's beneficial effects were also blocked by the postsynaptic antagonists SKF104078 and SKF104856, suggesting that clonidine acts by directly stimulating postsynaptic alpha-2 adrenoceptors. Beneficial doses of clonidine (0.01 mg/kg) and yohimbine (0.00001 mg/kg) were combined to see if they would produce additive effects on memory enhancement. This strategy was successful in young monkeys with intact NE systems but was not effective in the aged monkeys. These findings demonstrate that drugs that indirectly stimulate postsynaptic alpha-2 receptors by increasing NE release are not as reliable in aged monkeys as directly acting agonists that can replace NE at postsynaptic alpha-2 receptors.

Dose-dependent effects of the dopamine D1 receptor agonists A77636 or SKF81297 on spatial working memory in aged monkeys

With advancing age, monkeys develop deficits in spatial working memory resembling those induced by lesions of the prefrontal cortex (PFC). Aged monkeys also exhibit marked loss of dopamine from the PFC, a transmitter known to be important for proper PFC cognitive function. Previous results suggest that D1 agonist treatment can improve spatial working memory abilities in aged monkeys. However, this research was limited by the use of drugs with either partial agonist actions or significant D2 receptor actions. In our study, the selective dopamine D1 receptor full agonists A77636 and SKF81297 were examined in aged monkeys for effects on the working memory functions of the PFC. Both compounds produced a significant, dose-related effect on delayed response performance without evidence of side effects: low doses improved performance although higher doses impaired or had no effect on performance. Both the improvement and impairment in performance were reversed by pretreatment with the D1 receptor antagonist, SCH23390. These findings are consistent with previous results demonstrating that there is a narrow range of D1 receptor stimulation for optimal PFC cognitive function, and suggest that very low doses of D1 receptor agonists may have cognitive-enhancing actions in the elderly.