Investigating the status of biological stimuli as objects of attention in multiple object tracking

Background

Humans are able to track multiple simultaneously moving objects. A number of factors have been identified that can influence the ease with which objects can be attended and tracked. Here, we explored the possibility that object tracking abilities may be specialized for tracking biological targets such as people.

Methodology/Principal Findings

We used the Multiple Object Tracking (MOT) paradigm to explore whether the high-level biological status of the targets affects the efficiency of attentional selection and tracking. In Experiment 1, we assessed the tracking of point-light biological motion figures. As controls, we used either the same stimuli or point-light letters, presented in upright, inverted or scrambled configurations. While scrambling significantly affected performance for both letters and point-light figures, there was an effect of inversion restricted to biological motion, inverted figures being harder to track. In Experiment 2, we found that tracking performance was equivalent for natural point-light walkers and ‘moon-walkers’, whose implied direction was incongruent with their actual direction of motion. In Experiment 3, we found higher tracking accuracy for inverted faces compared with upright faces. Thus, there was a double dissociation between inversion effects for biological motion and faces, with no inversion effect for our non-biological stimuli (letters, houses).

Conclusions/Significance

MOT is sensitive to some, but not all naturalistic aspects of biological stimuli. There does not appear to be a highly specialized role for tracking people. However, MOT appears constrained by principles of object segmentation and grouping, where effectively grouped, coherent objects, but not necessarily biological objects, are tracked most successfully.     

Evidence for a Sex-Linked Haplo-Inviable Locus in the Cut-Singed Region of DROSOPHILA MELANOGASTER

Many cytologically normal and rearranged cut mutants have been reported, but no known deficiency involves both ct and its close neighbor, singed. This fact prompted an investigation of the mutational response of the ct–sn interval. Approximately 24,000 F₁ female progeny of 7-day-old males given 2000 or 3000r X-ray exposures were examined for the presence of newly induced mutations at the Notch, carmine, ct, and sn loci. One sn, 2 cm-ct, 31 N, and 33 ct mutants were found, indicating that the frequency of recovery of ct mutants is much greater than that of either cm or sn, as high even as N. Among the F₁ female progeny were two deficiency mutants that expressed both cm and ct (separated by 21 bands), but none expressed both ct and sn (separated by only 14 bands). Of the 18 cytologically analyzed ct mutants, two proved to be deficiencies; neither extended farther to the right than 7C1. No reported ct deficiency extends with certainty farther to the right than 7C4. This fact, together with the scarcity of sn deficiencies, suggests the presence of a haplo-insufficient locus between ct and sn that prevents recovery of ct-sn deficiencies. The analysis of the deficiency component of Tp sn^S93, a short transposition which moves most of the ct–sn interval from 7BC to 8D, proved the existence, just to the left of sn, of a haplo-inviable locus that prevents the development of females heterozygous for its deficiency.—A marked similarity between mutants at the N and ct loci was noted.     

Relative sensitivity of 32P-postlabelling of DNA and the autoradiographic UDS assay in the liver of rats exposed to 2-acetylaminofluorene (2AAF)

Groups of male Alderley Park rats were dosed concomitantly with 2-acetylaminofluorene (2AAF) by gavage at doses between 0.01 mg/kg and 40 mg/kg, and livers sampled 2-72 h later. The liver of one group of animals was perfused to yield hepatocytes which were assayed in vitro for unscheduled DNA synthesis (UDS) via incorporation of tritiated thymidine and autoradiography. DNA was extracted from the livers of the other group and DNA adduct levels determined using the 32P-postlabelling technique. The major C-8 2-aminofluorene/guanosine adduct and 3 minor adducts were quantitated, enabling the relative sensitivity of the 2 techniques to be compared. A dose- and time-related UDS response was observed, which, at the most sensitive time-point (12 h) enabled DNA repair to be discerned at a dose level of 0.1-1 mg/kg of 2AAF, a response classified as formally positive at 5 mg/kg 2AAF. Only the C-8 adduct, as determined by 32P-postlabelling, was discernible at 0.01 mg/kg of 2AAF, although other adducts were visible on autoradiograms at higher dose levels. It is concluded that as part of a well-defined dose response, UDS can be discerned with confidence for doses of 2AAF between approximately 0.1 and 5 mg/kg, and DNA adducts for doses of 2AAF between approximately 0.01 and 1 mg/kg. Discernible UDS for 2AAF in the rat liver is apparent at approximately 13 DNA (total) adducts/10(8) nucleotides, or approximately 8 DNA (C-8) adducts/10(8) nucleotides. The presumed C-8 2-acetylaminofluorene/guanosine adduct, prepared by reaction of 2-acetoxy-2-acetylaminofluorene (2AAAF) with DNA, was a significant but unreliable marker of 2AAF/DNA adducts in the rat liver in vivo. DNA repair did not appear to remove DNA adducts selectively, and adducts remained in DNA when discernible DNA repair had ceased.     

Motor and psycho-cognitive clinical types in adult metachromatic leukodystrophy: genotype/phenotype relationships?

Metachromatic leukodystrophy (MLD) is a recessive autosomal disease which is biochemically characterized by an accumulation of sulfatides (sulfogalactosylceramides) mainly in oligodendrocytes and macrophages/microglia. The deficient enzyme is a lysosomal hydrolase, cerebroside sulfate sulfatase (arylsulfatase A). MLD is both a dysmyelinating and a demyelinating disease. The main clinical forms are infantile or juvenile, but some forms appear at adulthood. This disease involves also neuronal cells as sulfatides are also present in neurons in which the defect in degradation occurs also. We have studied 12 cases of adult MLD and clearly distinguished two clinical forms. One of them was characterized by mainly central nervous system motor signs (pyramidal, cerebellar, and seldom dystonia) and a peripheral neuropathy. The other form always started by behavioural abnormalities with modifications of mood, peculiar social reactions; a progressive mental deterioration occurred also. The diagnosis of schizophrenia was often mentioned. Most of these patients remained for many years without any neurological symptoms, and the diagnosis was only made when neurological signs appeared, or when Magnetic Resonance Imaging (MRI) was performed. MRI showed a diffuse demyelination, bilateral and often symmetrical, which could be temporarily limited to the periventricular areas. The diagnosis of adult MLD was biochemical, evidencing the low activity of arylsulfatase A (ASA) and sulfatide accumulation. To determine the respective participation of neurons and glial cells in the physiopathology of both the motor forms and the psycho-cognitive forms, our first approach was to search for mutations differing according to the clinical status. Motor forms involved the major adult ASA mutation P426L in a homozygote form in contrast to psycho-cognitive forms which involved as a compound heterozygote a specific I179S mutation.     

Characterization of dog prenodal peripheral lymph lipoproteins. Evidence for the peripheral formation of lipoprotein-unassociated apoA-I with slow pre-beta electrophoretic mobility

Dog plasma and prenodal peripheral lymph apoA-I distribution was examined by nondenaturing gradient gel electrophoresis-immunoblot analysis. In control dogs, plasma apoA-I could be localized to two distinct populations of particles with modal diameters of 8.4 nm and 10.4 nm. The smaller sized population accounted for over 50% of plasma apoA-I. Peripheral lymph apoA-I distribution was significantly different. The percentage of apoA-I localized to the 10.4 nm population was reduced by 40% and the modal diameter of the smaller HDL apoA-I population was significantly decreased by 0.1 nm. Additionally, peripheral lymph apoA-I could be localized to particles smaller than albumin (lipoprotein-unassociated apoA-I). The presence of lipoprotein-unassociated apoA-I particles was confirmed by gel filtration chromatography. Immunoblots of column fractions subjected to agarose electrophoresis revealed that these particles had slow pre-beta electrophoretic mobility. In dogs fed an atherogenic diet, lipoprotein-unassociated apoA-I particles with slow pre-beta electrophoretic mobility could be found in both plasma and peripheral lymph. With increasing degree of hypercholesterolemia, the relative amount of plasma lipoprotein-unassociated apoA-I tended to increase. In peripheral lymph, an increasing degree of hypercholesterolemia was associated with a decrease in the relative amount of lipoprotein-unassociated apoA-I. Instead, a population of large apoA-I particles (11-25 nm) became increasingly prominent.     

Thymoquinone inhibits the CXCL12-induced chemotaxis of multiple myeloma cells and increases their susceptibility to Fas-mediated apoptosis

In multiple myeloma (MM), malignant plasma cells reside in the bone marrow, where they accumulate in close contact with stromal cells. The mechanisms responsible for the chemotaxis of malignant plasma cells are still poorly understood. Thus, we investigated the mechanisms involved in the chemotaxis of MDN and XG2 MM cell lines. Both cell lines strongly expressed CCR9, CXCR3 and CXCR4 chemokine receptors but only migrated toward CXCL12. Activation of CXCR4 by CXCL12 resulted in the association of CXCR4 with CD45 and activation of PLCβ3, AKT, RhoA, IκBα and ERK1/2. Using siRNA-silencing techniques, we showed CD45/CXCR4 association is essential for CXCL12-induced migration of MM cells. Thymoquinone (TQ), the major active component of the medicinal herb Nigella sativa Linn, has been described as a chemopreventive and chemotherapeutic compound. TQ treatment strongly inhibited CXCL12-mediated chemotaxis in MM cell lines as well as primary cells isolated from MM patients, but not normal PBMCs. Moreover, TQ significantly down-regulated CXCR4 expression and CXCL12-mediated CXCR4/CD45 association in MM cells. Finally, TQ also induced the relocalization of cytoplasmic Fas/CD95 to the membrane of MM cells and increased CD95-mediated apoptosis by 80%. In conclusion, we demonstrate the potent anti-myeloma activity of TQ, providing a rationale for further clinical evaluation.