The visual perception of long outdoor distances.

Many previous studies have investigated visual distance perception, especially for small to moderate distances. Few experiments, however, have evaluated the perception of large distances (e.g., 100 m or more). The studies that have been conducted have found conflicting results (diametrically opposite conclusions). In the current experiment, the functions relating actual and perceived distance were obtained for sixteen adult observers using the method of equal appearing intervals. These functions relating perceived and actual distance were obtained for outdoor viewing in a typical University environment-the experiment was conducted along a sidewalk adjacent to a typical street where campus buildings, trees, street signs, etc., were visible. The overall results indicated perceptual compression of distances in depth so that the stimulus distance intervals appeared significantly shorter than the actual (physical) distance intervals. It is important to note, however, that there were sizeable individual differences-the judgments of half of the observers were relatively accurate, whereas the judgments of the remaining half were inaccurate to varying degrees. The results of the experiment demonstrate that there is no single function that describes how human observers visually perceive large distance intervals in outdoor environments.

Aging and temporal integration in the visual perception of object shape.

It has been known for more than 160 years that highly occluded objects that would normally be visually unrecognizable can be successfully identified when they move. This anorthoscopic perception relies on the visual system's ability to integrate information over time to complete the perception of an entire object's shape. In this experiment, 16 younger and older adults (mean ages were 20.5 and 74.6 years, respectively) were familiarized with the (unoccluded) shapes of five naturally-shaped objects (bell peppers, Capsicum annuum) until they could be easily identified (i.e., with accuracies of at least 90 percent correct). All observers then viewed the stimulus objects anorthoscopically as they moved behind narrow slits; only small object fragments could be seen at any given time, because the objects were almost totally occluded from view. Even though the object identification performance for all observers was equivalent when whole object shapes were visible, a large age-related deficit in object identification emerged during anorthoscopic viewing such that the younger adults' identification performance was 45.4 percent higher than that of the older adults. This first ever study of aging and anorthoscopic perception demonstrates that there is an age-related deficit in performing the temporal integration needed for successful object recognition.

Aging and the detection of moving objects defined by common fate.

Grouping by common fate plays an important role in how human observers perceive environmental objects. In this study, the effect of aging upon the ability to utilize common fate was evaluated. Twenty-two younger and older adults (mean ages were 23.4 and 74.7 years, respectively) participated in two experiments. On any given trial, the participants sequentially viewed two apparent motion sequences and were required to indicate which temporal interval contained a coherently moving dotted line embedded in noisy random background motion. In Experiment 1, the number of dots defining the target was varied, while in Experiment 2, the target interpoint spacing was varied. The younger adults outperformed the older adults by 19.4 percent in Experiment 1 and 50.5 percent in Experiment 2. The older and younger adults were similarly affected by variations in the number of target dots and the target interpoint spacing. The individual older participants' object detection accuracies were highly correlated with their individual chronological ages, such that the performance of the younger old participants was much higher than that exhibited by the older old. Increases in age systematically affect the ability of older adults to detect and visually perceive objects defined by common fate.

Antioxidant defenses in the rat placenta in late gestation: increased labyrinthine expression of superoxide dismutases, glutathione peroxidase 3, and uncoupling protein 2.

Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders, most notably preeclampsia (PE) and intrauterine growth restriction (IUGR). Oxidative stress occurs when accumulation of reactive oxygen species (ROS) damages DNA, proteins and lipids, an outcome that is limited by antioxidant enzymes; mitochondrial uncoupling protein 2 (UCP2) may also limit oxidative stress by reducing ROS production. Here we characterized placental antioxidant defenses during normal gestation and following glucocorticoid-induced IUGR. Placentas were collected on Days 16 and 22 of normal rat pregnancy (term = Day 23) and at Day 22 after dexamethasone treatment from Day 13. Expression of several genes encoding antioxidant enzymes (Sod1, Sod2, Sod3, Cat, Gpx3, Txn1, Txnrd1, Txnrd2, and Txnrd3) and Ucp2 was measured by quantitative RT-PCR in the labyrinth (LZ) and junctional zones (JZ) of the placenta. Expression of Sod1 and Ucp2 mRNAs and the activity of xanthine oxidase, a source of ROS, all increased from Days 16 to 22 in both placental zones, whereas Sod2 and Gpx3 increased only in the rapidly growing LZ. In contrast, Sod3 and Txnrd1 expression fell in the LZ over this period, whereas total superoxide dismutase activity remained stable. Dexamethasone treatment reduced fetal-placental growth and LZ expression of Ucp2 but increased JZ expression of Txn1. Indices of placental oxidative damage (TBARS, F(2)-isoprostanes, and 8-OHdG) did not change with gestational age or dexamethasone, indicative of adequate antioxidant protection. Overall, our data suggest that the rat placenta is protected from oxidative stress by the dynamic zone- and stage-dependent expression of antioxidant defense genes.

Changes in the placental glucocorticoid barrier during rat pregnancy: impact on placental corticosterone levels and regulation by progesterone.

Glucocorticoid excess in utero inhibits fetal growth and programs adverse outcomes in adult offspring. Access of maternal glucocorticoid to the glucocorticoid receptor (NR3C1) in the placenta and fetus is regulated by metabolism via the 11beta-hydroxysteroid dehydrogenase (HSD11B) enzymes, as well as multidrug resistance P-glycoprotein (ABCB1)-mediated efflux of glucocorticoids from the syncytiotrophoblast. This study determined expression of genes encoding the two HSD11B isoforms (Hsd11b1 and Hsd11b2), the two ABCB1 isoforms (Abcb1a and Abcb1b), and Nr3c1 in the junctional and labyrinth zones of rat placentas at Days 16 and 22 of normal gestation (Day 23 is term). To assess possible regulation of the Hsd11b and Abcb1 isoforms by glucocorticoids and progesterone, their placental expression was also measured at Day 22 after partial progesterone withdrawal from Day 16 (maternal ovariectomy plus full estrogen and partial progesterone replacement) or after treatment with dexamethasone acetate (1 microg/ml of drinking water from Day 13). Expression of Hsd11b1 mRNA increased in the labyrinth zone (the site of maternal-fetal exchange) from Day 16 to Day 22, whereas that of Hsd11b2 fell dramatically. Consistent with these changes, corticosterone levels increased 10-fold in the labyrinth zone over this period. Expression of both Abcb1a and Abcb1b was markedly higher in the labyrinth zone compared with the junctional zone on both days, consistent with the proposed barrier role of ABCB1 in the placenta. Nr3c1 mRNA expression was similar in the two placental zones at Day 16 but increased 3-fold in the labyrinth zone by Day 22. Partial progesterone withdrawal increased Hsd11b1 mRNA and protein expression in the labyrinth zone but decreased Nr3c1 mRNA expression. These data show that the dynamic expression patterns of the placental HSD11Bs in late gestation are associated with dramatic shifts in placental corticosterone. Moreover, the late gestational rise in labyrinthine Hsd11b1 seems to be driven by the normal prepartum fall in progesterone level.

Reiterated Wnt signaling during zebrafish neural crest development.

While Wnt/beta-catenin signaling is known to be involved in the development of neural crest cells in zebrafish, it is unclear which Wnts are involved, and when they are required. To address these issues we employed a zebrafish line that was transgenic for an inducible inhibitor of Wnt/beta-catenin signaling, and inhibited endogenous Wnt/beta-catenin signaling at discrete times in development. Using this approach, we defined a critical period for Wnt signaling in the initial induction of neural crest, which is distinct from the later period of development when pigment cells are specified from neural crest. Blocking Wnt signaling during this early period interfered with neural crest formation without blocking development of dorsal spinal neurons. Transplantation experiments suggest that neural crest precursors must directly transduce a Wnt signal. With regard to identifying which endogenous Wnt is responsible for this initial critical period, we established that wnt8 is expressed in the appropriate time and place to participate in this process. Supporting a role for Wnt8, blocking its function with antisense morpholino oligonucleotides eliminates initial expression of neural crest markers. Taken together, these results demonstrate that Wnt signals are critical for the initial induction of zebrafish neural crest and suggest that this signaling pathway plays reiterated roles in its development.

Real-time visualization of mycobacterium-macrophage interactions leading to initiation of granuloma formation in zebrafish embryos.

Infection of vertebrate hosts with pathogenic Mycobacteria, the agents of tuberculosis, produces granulomas, highly organized structures containing differentiated macrophages and lymphocytes, that sequester the pathogen. Adult zebrafish are naturally susceptible to tuberculosis caused by Mycobacterium marinum. Here, we exploit the optical transparency of zebrafish embryos to image the events of M. marinum infection in vivo. Despite the fact that the embryos do not yet have lymphocytes, infection leads to the formation of macrophage aggregates with pathological hallmarks of granulomas and activation of previously identified granuloma-specific Mycobacterium genes. Thus, Mycobacterium-macrophage interactions can initiate granuloma formation solely in the context of innate immunity. Strikingly, infection can redirect normal embryonic macrophage migration, even recruiting macrophages seemingly committed to their developmentally dictated tissue sites.