多重上市股价异常效应的影响因素——来自中国A、B股证券市场的证据

实证检验了多重上市的股价异常效应及其影响因素。结果表明,多重上市的股价异常效应并非市场过度反应的结果,而与A、B股的市场分割、发行价格与原股票价格的差异、上市前后流动性的变化紧密联系。另外,A股市场多重上市的股价异常效应主要表现在招股公告前,B股市场多重上市的股价异常效应则主要表现在招股公告后。从股东构成、时间因素、散户投资者的损失厌恶心理方面探讨了以上不对称反应模式的原因。     

亨施自述

在我们极其复杂和不断变化的世界里，知悉某些物理量能用很高的精确度来测量和预言，是一件人欣慰的事。精确测量作为物理学中最美的一个方面永远吸引着我。使用更好的测量工具，人们能够看到以前无人见过的地方。不止一次，测量值与理论值之间似乎微不足道的差异导致了基础知识领域里的重要进展。现代科学的诞生本身便是与精确的测量技术密切相关。     

Microbial starch-binding domains are superior to granule-bound starch synthase I for anchoring luciferase to potato starch granules

Microbial starch-binding domains (SBD) and granule-bound starch synthase I (GBSSI) are proteins which are accumulated in potato starch granules. The efficiency of SBD and GBSSI for targeting active luciferase reporter proteins to granules during starch biosynthesis was compared. GBSSI or SBD sequences were fused to the N- or C-terminus of the luciferase (LUC) gene, via an artificial Pro-Thr encoding linker sequence. The genes were introduced into an amylose-free (amf) potato mutant. It appeared that SBD was superior to GBSSI as a targeting sequence, mainly because the luciferase retained higher activity in the SBD-containing fusion proteins than in the GBSSI-containing ones.     

Mutations in genes encoding melanosomal proteins cause pigmentary glaucoma in DBA/2J mice.

Pigmentary glaucoma is a significant cause of human blindness. Abnormally liberated iris pigment and cell debris enter the ocular drainage structures, leading to increased intraocular pressure (IOP) and glaucoma. DBA/2J (D2) mice develop a form of pigmentary glaucoma involving iris pigment dispersion (IPD) and iris stromal atrophy (ISA). Using high-resolution mapping techniques, sequencing and functional genetic tests, we show that IPD and ISA result from mutations in related genes encoding melanosomal proteins. IPD is caused by a premature stop codon mutation in the Gpnmb (GpnmbR150X) gene, as proved by the occurrence of IPD only in D2 mice that are homozygous with respect to GpnmbR150X; otherwise, similar D2 mice that are not homozygous for GpnmbR150X do not develop IPD. ISA is caused by the recessive Tyrp1b mutant allele and rescued by the transgenic introduction of wildtype Tyrp1. We hypothesize that IPD and ISA alter melanosomes, allowing toxic intermediates of pigment production to leak from melanosomes, causing iris disease and subsequent pigmentary glaucoma. This is supported by the rescue of IPD and ISA in D2 eyes with substantially decreased pigment production. These data indicate that pigment production and mutant melanosomal protein genes may contribute to human pigmentary glaucoma. The fact that hypopigmentation profoundly alleviates the D2 disease indicates that therapeutic strategies designed to decrease pigment production may be beneficial in human pigmentary glaucoma.     

应用激光闪光法测量薄膜材料的热扩散率

目的是将用于测量片状试样的热扩散率的激光闪光法推广至测量薄膜试样。应用 1 5纳秒脉冲 Nd:YAG激光及响应时间 0 .9微秒的 (Hg,Cd) Te红外探测器等建立了闪光法热扩散率测量系统 ,并应用此系统对微米量级厚度的不锈钢薄膜进行了测量。同时针对将激光闪光法应用于薄膜时所出现的问题 ,如激光的有限脉冲时间及有限吸收厚度效应 ,测量系统的滞后效应 ,以及增强红外吸收及辐射用表面黑化膜的影响进行了分析并提出了解决方法     

Palaeolake and palaeoenvironment between 42 and 18 kaBP in tengger desert, NW China

Comprehensive field investigations and laboratory analyses show that palaeolakes, including fresh- mesohaline water Megalake Tengger and other semi-con- nected, isolated water bodies, during late Pleistocene covered an area of more than 20000 km², which is more than half of the Tengger Desert in NW China. Stratigraphic correlation and chronological evidence indicate that before ca. 42000 aBP the area was more arid. The palaeolakes started to develop around 40000 uncal. ¹⁴C aBP but until 37000 ¹⁴C aBP their scope was limited. High water levels established from 35000 ¹⁴C aBP lasted until 22000 ¹⁴CaBP. Lake levels regressed between 22000 and 20000 ¹⁴C aBP but transgressed from 20000 to 18600 ¹⁴C aBP. Subsequently, water level declined further and the Megalake Tengger finally desiccated at around 18000 ¹⁴C aBP. Megalake Tengger possessed a fresh-mesohaline water property, implying that the regional precipitation increased significantly. During the period of Megalake Tengger, the climate was warmer-humid than present. The annual rainfall was 250 to 350 mm more than that of today and the temperature was 1.5 to 3.0℃ higher.     

Sox9 induces testis development in XX transgenic mice.

Mutations in SOX9 are associated with male-to-female sex reversal in humans. To analyze Sox9 function during sex determination, we ectopically expressed this gene in XX gonads. Here, we show that Sox9 is sufficient to induce testis formation in mice, indicating that it can substitute for the sex-determining gene Sry.     

Mutations in a human homologue of Drosophila crumbs cause retinitis pigmentosa (RP12).

Retinitis pigmentosa (RP) comprises a clinically and genetically heterogeneous group of diseases that afflicts approximately 1.5 million people worldwide. Affected individuals suffer from a progressive degeneration of the photoreceptors, eventually resulting in severe visual impairment. To isolate candidate genes for chorioretinal diseases, we cloned cDNAs specifically or preferentially expressed in the human retina and the retinal pigment epithelium (RPE) through a novel suppression subtractive hybridization (SSH) method. One of these cDNAs (RET3C11) mapped to chromosome 1q31-q32.1, a region harbouring a gene involved in a severe form of autosomal recessive RP characterized by a typical preservation of the para-arteriolar RPE (RP12; ref. 3). The full-length cDNA encodes an extracellular protein with 19 EGF-like domains, 3 laminin A G-like domains and a C-type lectin domain. This protein is homologous to the Drosophila melanogaster protein crumbs (CRB), and denoted CRB1 (crumbs homologue 1). In ten unrelated RP patients with preserved para-arteriolar RPE, we identified a homozygous AluY insertion disrupting the ORF, five homozygous missense mutations and four compound heterozygous mutations in CRB1. The similarity to CRB suggests a role for CRB1 in cell-cell interaction and possibly in the maintenance of cell polarity in the retina. The distinct RPE abnormalities observed in RP12 patients suggest that CRB1 mutations trigger a novel mechanism of photoreceptor degeneration.