视知觉学习对于识别动态随机点立体图深度运动方向的作用

立体视觉不仅指对静态深度信息的感知,也包括对物体在三维空间中的运动方向的判断。本研究记录了人眼对于动态随机点图运动方向的辨别能力以及视觉训练在提高对动态信息分辨能力的作用。实验结果表明,对于没有任何相关经验的视力正常的受试者,很难分辨出动态随机点的深度运动方向,而视觉训练可以大大提高人眼对物体深度运动方向判断的敏感度。此外,这种视觉训练所达到的效果具有较长时间的持续性（至少6个月）。这种通过视觉训练提高受试者对立体运动信息的敏感度的方式为立体视觉相关的实验和研究提供了新的视角。     

The human placental anti-aggregating factor is neither prostacyclin, nor a prostacyclin metabolite

Using PGH₂ as substrate, we have previously demonstrated that human placenta synthetizes mainly PGE₂, TxB₂ and PGD₂(1,2). Other reports have shown that placental tissue generates a substance which inhibits ADP-induced platelet aggregation and which was supposed to be PGI₂ (3). The present study indicates that the stability of that substance is different from the stability of prostacyclin (released by umbilical artery pieces). By GC-MS and multiple ion-monitoring, we have shown the presence of 6 keto-PGF_1α (the stable metabolite of PGI₂) in the umbilical artery incubation medium, while no trace of 6-keto-PGF_1α could be found in the placental medium. No conversion of AA to 6-keto-PGF_1α by placental microsomes was observed, even in the presence of antioxidants. The placenta possesses, in addition to the known 15-OH-PGDH and Δ-13 reductase activities, a weak 9 OH pGDH which is specific for PGF_2α (and not PGI₂ nor 6-keto-PGF_1α). GC-MS analysis is showed that the expected metabolites of PGI₂ through those three enzymes were not found in the placental medium, indicating that neither PGI₂ synthesis nor metabolism could be demonstrated in the placenta.     

Evidence of functional redundancy between MID proteins: implications for the presentation of Opitz syndrome

Opitz G/BBB syndrome (OS) is a congenital defect characterized by hypertelorism and hypospadias, but additional midline malformations are also common in OS patients. X-linked OS is caused by mutations in the ubiquitin ligase MID1. In chick, MID1 is involved in left-right determination: a mutually repressive relationship between Shh and cMid1 in Hensen's node plays a key role in establishing the avian left-right axis. We have utilized our existing knowledge of the molecular basis of avian L/R determination to investigate the possible existence of functional redundancy between MID1 and its close homologue MID2. The expression of cMid2 overlaps with that of cMid1 in the node, and we demonstrate that MID2 can both mimic MID1 function as a right side determinant and rescue the laterality defects caused by knocking down endogenous MID proteins in the node. Our results show that MID2 is able to compensate for an absence in MID1 during chick left-right determination and may explain why OS patients do not suffer laterality defects despite the association between midline and L/R development. The demonstration of functional redundancy between MID1 and MID2 in the node provides supports for the hypothesis that partial functional redundancy between MID proteins in other developing structures contributes to the wide variability of OS phenotype.