Perceived pattern regularity computed as a summary statistic: implications for camouflage.

Why do the equally spaced dots in figure 1 appear regularly spaced? The answer 'because they are' is naive and ignores the existence of sensory noise, which is known to limit the accuracy of positional localization. Actually, all the dots in figure 1 have been physically perturbed, but in the case of the apparently regular patterns to an extent that is below threshold for reliable detection. Only when retinal pathology causes severe distortions do regular grids appear perturbed. Here, we present evidence that low-level sensory noise does indeed corrupt the encoding of relative spatial position, and limits the accuracy with which observers can detect real distortions. The noise is equivalent to a Gaussian random variable with a standard deviation of approximately 5 per cent of the inter-element spacing. The just-noticeable difference in positional distortion between two patterns is smallest when neither of them is perfectly regular. The computation of variance is statistically inefficient, typically using only five or six of the available dots.

Dark scene elements strongly influence cuttlefish camouflage responses in visually cluttered environments.

This study investigated how cuttlefish (Sepia officinalis) camouflage patterns are influenced by the proportions of different gray-scales present in visually cluttered environments. All experimental substrates comprised spatially random arrays of texture elements (texels) of five gray-scales: Black, Dark gray, Gray, Light gray, and White. The substrates in Experiment 1 were densely packed arrays of square texels that varied over 4 sizes in different conditions. Experiment 2 used substrates in which texels were disks separated on a homogeneous background that was Black, Gray or White in different conditions. In a given condition, the histogram of texel gray-scales was varied across different substrates. For each of 16 cuttlefish pattern response statistics c, the resulting data were used to determine the strength with which variations in the proportions of different gray-scales influenced c. The main finding is that darker-than-average texels (i.e., texels of negative contrast polarity) predominate in controlling cuttlefish pattern responses in the context of cluttered substrates. In Experiment 1, for example, substrates of all four texel-sizes, activation of the cuttlefish "white square" and "white head bar" (two highly salient skin components) is strongly influenced by variations in the proportions of Black and Dark gray (but not Gray, Light gray, or White) texels. It is hypothesized that in the context of high-variance visual input characteristic of cluttered substrates in the cuttlefish natural habitat, elements of negative contrast polarity reliably signal the presence of edges produced by overlapping objects, in the presence of which disruptive pattern responses are likely to achieve effective camouflage.

Predicting the motion after-effect from sensitivity loss.

The widely accepted disinhibition theory of the motion after-effect (MAE) proposes that the balance point of an opponent mechanism is changed by directional adaptation. To see if the post-adaptation balance point could be predicted from contrast adaptation, we measured threshold-vs-contrast (i.e., T-vs-C or dipper) functions, before and after adaptation to moving gratings. For test stimuli moving in the same direction, adaptation shifted the point of maximum facilitation (i.e., the dip) upwards and rightwards. For tests moving in the opposite direction, adaptation produced a similar, but smaller, shift. These shifts are consistent with a change in divisive gain control. They are also consistent with subtractive inhibition followed by half-wave rectification. We attempted to use transducer functions derived from these data to predict the strength of the MAE. When combined, gratings moving in the adapted and opposite directions appeared perfectly balanced (i.e., counterphasing) when the latter was given approximately 2% more contrast than was predicted on the basis of the derived transducers. This small under-prediction may be indicative of sensory recalibration. Finally, we found that adaptation did not alter the fact that low-contrast stimuli could be detected and their direction identified with similar accuracy. We conclude that both static and dynamic forms of MAE are primarily caused by a decreased sensitivity in directionally tuned mechanisms, as proposed by the disinhibition theory.

Increased inosine-5'-phosphate dehydrogenase gene expression in solid tumor tissues and tumor cell lines.

Inosine-5'-phosphate (IMP) dehydrogenase, a regulatory enzyme of guanine nucleotide biosynthesis, may play a role in cell proliferation and malignancy. To assess this role we examined IMP dehydrogenase expression in a series of human solid tumor tissues and tumor cell lines in comparison with their normal counterparts. Increased IMP dehydrogenase gene expression was observed in brain tumors relative to normal brain tissue and in sarcoma cells relative to normal fibroblasts. Similarly, in several B- and T-lymphoid leukemia cell lines, elevated levels of IMP dehydrogenase mRNA and cellular enzyme were observed in comparison with the levels in peripheral blood lymphocytes. These results are consistent with an association between increased IMP dehydrogenase expression and either enhanced cell proliferation or malignant transformation.

Alteration in glycosphingolipid pattern during phorbol-12-myristate-13-acetate-induced cell differentiation in human T-lymphoid leukemia cells.

We analyzed the patterns of glycosphingolipids (GSLs) from a line of cells derived from a clone of the human T-cell leukemia cells (CEM) that had been induced to differentiate by phorbol-12-myristate-13-acetate (PMA) into cells with a suppressor-like phenotype. We characterized the differentiation state of the cells by immunofluorescence by using anti-cell surface differentiation-specific monoclonal antibodies (OKT3, OKT4, OKT6, and OKT8). The GSLs were extracted and separated by thin-layer chromatography and the individual bands were quantitated by a dual-wavelength densitometer or by autoradiography of GSLs labeled with [14C]glucosamine and [14C]galactose. Treatment of the CEM cells with 0.16-16 nM PMA for 6 h to 6 days resulted in a dose- and time-dependent increase in the amount of two neutral GSLs [ceramide monohexoside and ceramide dihexoside] and three gangliosides [monosialoganglioside (GM3), sialosylparagloboside, and disialoganglioside (GD3)]. The increase in the neutral GSLs after PMA treatment reached its maximum at 30 h while GM3 peaked at 96 h. The increases in GM3 and sialosylparagloboside are presumably due to an increase in their synthesis levels because PMA promoted an elevated incorporation of glucosamine and galactose into these GSLs. The increase in the amount of GD3, on the other hand, is due to either a decrease in its degradation or use in other metabolic pathways because no detectable increase in glucosamine and galactose incorporation into this ganglioside could be found. Incubation of control or PMA-induced CEM cells with GM3 fractions purified from either CEM cells, human brain, or dog erythrocytes caused a reduction in cell growth and prevented the increase in reactivity of the induced cells with the OKT3 antibody. Incubation with semisynthetic ceramide dihexoside, however, prevented the decrease in reactivity with the OKT4 antibody. The observed changes in GSL patterns during PMA-induced differentiation of the CEM cells into suppressor-like cells and the inhibition of CEM cell growth by GM3 fractions suggest that the GSLs play a role in the control of cell growth and differentiation in the PMA-treated CEM cells.

Novobiocin- and phorbol-12-myristate-13-acetate-induced differentiation of human leukemia cells associated with a reduction in topoisomerase II activity.

Studies were conducted to determine the possible involvement of DNA topoisomerase II (Topo II) in the induction of differentiation in two human promyelocytic HL-60 leukemia cell variants that are either susceptible or resistant to differentiation induced by phorbol-12-myristate-13-acetate (PMA), a protein kinase C activator. The acquisition of maturation markers and changes in the activity, level, and phosphorylation of Topo II were determined after treatment with either novobiocin, a Topo II inhibitor, or PMA. Novobiocin at 50-150 microM induced differentiation in the HL-205 cells but not in the HL-525 cells, although both cell types were equally susceptible to novobiocin-evoked cytotoxicity. In both cell types, novobiocin induced similar reductions in topoisomerase I activity but different reductions in Topo II activity. Treatment with novobiocin at 150 microM for 6 h or at 2 mM for 30 min resulted in a 4-fold or higher reduction in Topo II activity in the differentiation-susceptible HL-205 cells but not in the differentiation-resistant HL-525 cells. A differential response in Topo II activity was also observed after treatment with PMA. The novobiocin-evoked decrease in Topo II activity seems to be due to an enhanced enzyme proteolysis, whereas the PMA-elicited decrease in Topo II activity is associated with an increase in Topo II phosphorylation. 1-(5-Isoquinolinesulfonyl)-2-methylpiperazine, which is an inhibitor of protein kinases, including protein kinase C, diminished the novobiocin-elicited proteolysis of Topo II and the PMA-induced Topo II phosphorylation, as well as the decrease in Topo II activity and the acquisition of differentiation markers induced by either novobiocin or PMA. These results suggest that induction of differentiation in HL-60 cells by novobiocin or PMA is associated with a reduction in Topo II activity, mediated directly or indirectly by a protein kinase(s), perhaps protein kinase C.

Glycosphingolipid patterns in human promyelocytic HL-60 leukemia cells susceptible or resistant to differentiation induction by phorbol 12-myristate 13-acetate.

The patterns of glycosphingolipids (GSLs) were analyzed in an HL-60 cell variant, HL-205, which is susceptible to phorbol 12-myristate 13-acetate (PMA)-induced monocyte/macrophage differentiation, and in an HL-60 cell variant, HL-525, which is resistant to such differentiation. The amounts and types of the GSLs were similar in both the HL-205 and HL-525 cells and they resemble those of granulocytes. Treatment with 3 nM PMA caused the susceptible HL-205 cells (but not the resistant cells) to acquire a new GSL pattern which resembles that of monocytes. This new pattern was characterized by increases in the level of a neutral GSL, Gb3Cer, from trace levels to 0.05 mg/10(9) cells and of an acidic GSL, GM3 ganglioside, from 0.03 to 0.33 mg/10(9) cells. The increases in the level of this ganglioside were found to be due to an increase in CMP-N-acetylneuraminic acid:lactosylceramide sialyltransferase activity. These results indicate an association between PMA-induced terminal differentiation along the monocyte/macrophage cell lineage and PMA-evoked increases in specific GSLs, GM3 in particular, which is due to a rise in the activity of its synthetic enzyme.

Animal models of male infertility: mice bearing single-gene mutations that induce infertility.

Genetically defined mouse models of male infertility are described in the present report. The mice were rendered infertile by one of the following gene mutations: Ames dwarf, dwarf, flipper-arm, hightail, hypothyroid, little, pygmy, stubby. The effects of each gene mutation on testicular steroidogenesis and spermatogenesis were elucidated by a comparison of the mutant mice to their normal siblings. Testicular steroidogenesis was assessed directly by determining steroid secretion by testes perfused in vitro. The study provides the first comprehensive assessment of testicular function in the mutant mice. The eight gene mutations can be classified into two groups based on the results. One group of gene mutations (Ames dwarf, dwarf, flipper-arm, pygmy) specifically depress spermatogenesis and testicular steroidogenesis. The infertility of these mutant mice can be linked to the lowered total sperm production. The second group of gene mutations (hightail, hypothyroid, little, stubby) do not specifically depress either spermatogenesis or testosterone secretion. Subsequently, the etiology of the male infertility of the second group of mutant mice is unknown. We propose that these mutant mice provide valuable experimental tools for the study of male infertility and male reproduction.

Cytoplasmic malic enzyme and testicular steroidogenesis in mice.

The malate shuttle has been hypothesized as a source of the intramitochondrial NADPH required for cholesterol side-chain cleavage. In the present report, the role of the malate shuttle in testicular steroidogenesis was investigated by employing mouse mutants deficient in cytoplasmic malic enzyme, a required component of the shuttle. Androgen-dependent parameters plus testosterone secretion by in vitro perfused testes were similar for the mutants and their normal siblings. The data suggest that an active malate shuttle is not required for cholesterol side-chain cleavage in mouse testes.

Animal models of physiologic markers of male reproduction: genetically defined infertile mice.

The present report focuses on novel animal models of male infertility: genetically defined mice bearing single-gene mutations that induce infertility. The primary goal of our investigations was to identify the reproductive defects in these mutant mice. The phenotypic effects of the gene mutations were deciphered by comparing the mutant mice to their normal siblings. Initially testicular steroidogenesis and spermatogenesis were investigated. The physiologic markers for testicular steroidogenesis were steroid secretion by testes perifused in vitro, seminal vesicle weight, and Leydig cell histology. Spermatogenesis was evaluated by the enumeration of homogenization-resistant sperm/spermatids in testes and by morphometric analyses of germ cells in the seminiferous epithelium. If testicular function appeared normal, we investigated the sexual behavior of the mice. The parameters of male sexual behavior that were quantified included mount patency, mount frequency, intromission latency, thrusts per intromission, ejaculation latency, and ejaculation duration. Females of pairs breeding under normal circumstances were monitored for the presence of vaginal plugs and pregnancies. The patency of the ejaculatory process was determined by quantifying sperm in the female reproductive tract after sexual behavior tests. Sperm function was studied by quantitatively determining sperm motility during videomicroscopic observation. Also, the ability of epididymal sperm to function within the uterine environment was analyzed by determining sperm capacity to initiate pregnancy after artificial insemination. Together, the experimental results permitted the grouping of the gene mutations into three general categories. We propose that the same biological markers used in the reported studies can be implemented in the assessment of the impact that environmental toxins may have on male reproduction.

Assessment of testicular testosterone production and Leydig cell structure.

Advances in two techniques have made the problem of assessing the acute and/or chronic effects of toxic agents on Leydig cell structure and testosterone synthesis and secretion amenable to study. First, in vitro testicular perfusion has been perfected to a point where it closely resembles in situ testosterone secretion. Second, now it is possible to quantify the proportion of Leydig cell cytoplasm occupied by the cellular organelles which contain steroidogenic enzymes. Herein, we report that inhibition of Leydig cell steroidogenic enzymes is reflected by reduced testosterone secretion by in vitro perfused rat and rabbit testes. Moreover, the activity of specific steroidogenic reactions can be monitored by measuring the secretion of reaction substrate(s) and product(s) from in vitro perfused testes. Testosterone secretion by in vitro perfused testes from five species is highly and positively correlated with the volume density of smooth endoplasmic reticulum in Leydig cell cytoplasm. Exploitation of these findings will allow toxicologists to quantitatively assess the effect of toxicants on Leydig cell testosterone biosynthesis and secretion, to identify the specific steroidogenic enzymes affected, to assess whether the membranous environment of the steroidogenic enzymes is compromised, and perhaps even to predict the deleterious effect of a toxic agent on Leydig cell steroidogenic function from a stereological assessment of Leydig cell ultrastructure.

Glycosphingolipid patterns of peripheral blood lymphocytes, monocytes, and granulocytes are cell specific.

We analyzed the amounts and types of glycosphingolipids (GSLs) from peripheral blood lymphocytes, monocytes, and granulocytes isolated by counter-current elutriation. The three cell types contained different amounts of neutral and acidic GSLs. The highest amount of neutral GSLs (109 micrograms/10(8) cells) was found in granulocytes, with considerably less found in monocytes (11 micrograms/10(8) cells) and lymphocytes (4 micrograms/10(8) cells). The neutral GSLs were composed of four types of lipids, GL1 through GL4 (mono-, di-, tri-, and tetraosylceramide). The highest percentage of GL1 was detected in lymphocytes and the lowest percentage in granulocytes, with the reverse order observed for GL2. GL3 and GL4, which were minor components of the neutral GSLs, were highly cell specific, with lymphocytes containing GL3 and GL4 of the globo series, granulocytes containing GL3 and GL4 of the lacto or neolacto series, and monocytes containing GL3 and GL4 of both types. The acidic GSL, sialosyl hexaosylceramide (lacto-series), was abundant in granulocytes but not in monocytes or lymphocytes. Another ganglioside, GM3, although present in all three cell types, was most abundant in monocytes and lymphocytes, whereas sialosyl paragloboside was higher in granulocytes than in lymphocytes and monocytes. These results indicate that peripheral blood lymphocytes, monocytes, and granulocytes have distinct "GSL fingerprints."

Oligotriche and quaking gene mutations. Phenotypic effects on mouse spermatogenesis and testicular steroidogenesis.

The phenotypic actions of the oligotriche gene mutation on testicular function have not been elucidated, although it is known that male mice homozygous for the mutation are infertile. In the present study, the effect of the oligotriche gene mutation on mouse testicular function was analyzed by comparing normal and mutant mice. Spermatogenesis was analyzed by enumerating germ cells in seminiferous tubules at specific stages of spermatogenesis and by electron microscopy. Steroidogenic potential was estimated by radioimmunometric determination of testosterone secreted by testes perfused in vitro. Parallel studies were completed for male mice homozygous for the quaking gene mutation, a mutation known to cause male mouse sterility by disrupting sperm tail development. The experimental results suggest that the oligotriche and quaking gene mutations interfere with sperm tail formation by different mechanisms. Testicular steroidogenesis was not affected by either gene mutation. The results provide the first evidence that the oligotriche gene mutation induces male mouse sterility by effecting the complete absence of a sperm tail. This phenotypic action is different from that of the quaking gene mutation.

Genetically defined mouse models of male infertility.

The review has four objectives. The first objective is to summarize our studies of gene mutations that induce infertility in male mice. The second objective is to stress the power of mouse genetics and its application to male reproductive biology. The third objective is to provide useful references to the literature about gene mutations affecting male mouse fertility. Our goal is to cite references that can be used as a starting point for reading, not to present a comprehensive list of references. The fourth objective is to present a summary of selected data collected from mice representing 21 mouse strains.

The size-tuning of the face-distortion after-effect.

Recently, Webster and MacLin demonstrated a face-distortion after-effect (FDAE) for both upright and inverted faces: adaptation to a distorted face makes a normal face appear distorted in the direction opposite to the adapting direction. Neurophysiological studies (e.g. Experimental Brain Research 65 (1986) 38) show that face-selective neurons in the superior temporal sulcus (STS) are remarkably size-invariant in their responses. If the site of adaptation underlying the FDAE is the homologous neuron population in human vision, then the FDAE should also be highly tolerant to changes in size between adapting and test faces. Here, we test this prediction. Observers were adapted to distorted upright/inverted faces of three different sizes (3.3 degrees x 3.7 degrees, 6.6 degrees x 7.5 degrees, and 13.1 degrees x 14.8 degrees ). For adapting faces of all three sizes, observers adjusted test faces of all three sizes until they appeared normal. Significant FDAEs were observed in all conditions. For both upright and inverted faces, FDAEs were approximately twice as strong when adapting and test faces were the same size than when they differed by even a single octave in size. The magnitudes of FDAEs were comparable for upright and inverted faces. The larger FDAEs for same-size adapting and test faces suggest that part of the FDAE derives from a neuron population with narrow size-tuning. However, the significant FDAEs obtained for adapting and test images differing by two octaves implicate a different neuron population with broad size-tuning, possibly the human homolog of the face-selective neuron population in monkey STS.

The dimensionality of texture-defined motion: a single channel theory.

We examine apparent motion carried by textural properties. The texture stimuli consist of a sequence of grating patches of various spatial frequencies and amplitudes. Phases are randomized between frames to insure that first-order motion mechanisms directly applied to stimulus luminance are not systematically engaged. We use ambiguous apparent motion displays in which a heterogeneous motion path defined by alternating patches of texture s (standard) and texture v (variable) competes with a homogeneous motion path defined solely by patches of texture s. Our results support a one-dimensional (single-channel) model of motion-from-texture in which motion strength is computed from a single spatial transformation of the stimulus--an activity transformation. The value assigned to a point in space-time by this activity transformation is directly proportional to the modulation amplitude of the local texture and inversely proportional to local spatial frequency (within the range of spatial frequencies examined). The activity transformation is modeled as the rectified output of a low-pass spatial filter applied to stimulus contrast. Our data further suggest that the strength of texture-defined motion between a patch of texture s and a patch of texture v is proportional to the product of the activities of s and v. A strongly counterintuitive prediction of this model borne out in our data is that motion between patches of different texture can be stronger than motion between patches of similar texture (e.g. motion between patches of a low contrast, low frequency texture 1 and patches of high contrast, high frequency texture h can be stronger than motion between patches of similar texture h).

Measuring the spatial frequency selectivity of second-order texture mechanisms.

Recent investigations of texture and motion perception suggest two early filtering stages: an initial stage of selective linear filtering followed by rectification and a second stage of linear filtering. Here we demonstrate that there are differently scaled second-stage filters, and we measure their contrast modulation sensitivity as a function of spatial frequency. Our stimuli are Gabor modulations of a suprathreshold, bandlimited, isotropic carrier noise. The subjects' task is to discriminate between two possible orientations of the Gabor. Carrier noises are filtered into four octave-wide bands, centered at m = 2, 4, 8, and 16 c/deg. The Gabor test signals are w = 0.5, 1, 2, 4 and 8 c/deg. The threshold modulation of the test signal is measured for all 20 combinations of m and w. For each carrier frequency m, the Gabor test frequency w to which subjects are maximally sensitive appears to be approximately 3-4 octaves below m. The consistent m x w interaction suggests that each second-stage spatial filter may be differentially tuned to a particular first-stage spatial frequency. The most sensitive combination is a second-stage filter of 1 c/deg with first-stage inputs of 8-16 c/deg. We conclude that second-order texture perception appears to utilize multiple channels tuned to spatial frequency and orientation, with channels tuned to low modulation frequencies appearing to be best served by carrier frequencies 8 to 16 times higher than the modulations they are tuned to detect.

Perception of apparent motion between dissimilar gratings: spatiotemporal properties.

What determines the strength of texture-defined apparent motion perception when the stimulus has no net directional energy in the Fourier domain? In a previous paper [Werkhoven, Sperling & Chubb (1993) Vision Research, 33, 463-485] we demonstrated the counterintuitive finding that the correspondence in spatial frequency and in modulation amplitude between neighboring patches of texture in a spatiotemporal motion path are irrelevant to motion strength. Instead, we found strong support for what we call a single channel or one-dimensional motion computation: a simple nonlinear transformation of the image, followed by standard motion analysis. Here, we further studied the dimensionality of the motion computation in a parameter space that includes texture orientation and stimulus display rate in addition to texture spatial frequency and modulation amplitude. We used ambiguous motion displays in which one motion path, consisting of patches of nonsimilar texture, competes with another motion path comprised entirely of similar texture patches. The data show that motion between dissimilar patches of texture that are orthogonally oriented, have a two octave difference in spatial frequency and differ 50% in modulation amplitude can easily dominate motion between similar patches of texture. A single channel accounts for more than 70% of texture-from-motion strength for the parameter space examined and this channel is invariant for stimulus display rates varying over a four-fold range.

Every discrete, finite image is uniquely determined by its dipole histogram.

A finite image I is a function assigning colors to a finite, rectangular array of discrete pixels. Thus, the information directly encoded by I is purely locational. Such locational information is of little visual use in itself: perception of visual structure requires extraction of relational image information. A very elementary form of relational information about I is provided by its dipole histogram DI. A dipole is a triple, ((dx, dy), alpha, beta), with dx and dy horizontal and vertical, integer-valued displacements, and alpha and beta colors. For any such dipole, DI((dx, dy), alpha, beta) gives the number of pixel pairs ((x1, y1), (x2, y2)) of I such that I[x1, y1] = alpha, I[x2, y2] = beta, and, (x2, y2) - (x1, y1) = (dx, dy). Note that DI explicitly encodes no locational information. Although DI is uniquely determined by (and easily constructed from) I, it is not obvious that I is uniquely determined by DI. Here we prove that any finite image I is uniquely determined by its dipole histogram, DI. Two proofs are given; both are constructive, i.e. provide algorithms for reconstructing I from DI. In addition, a proof is given that any finite, two-dimensional image I can be constructed using only the shorter dipoles of I: those dipoles ((dx, dy), alpha, beta) that have magnitude of dx < or = ceil((# columns in I)/2) and magnitude of dy < or = ceil((# rows in I)/2), where ceil(x) denotes the greatest integer < or = x.

Variance of high contrast textures is sensed using negative half-wave rectification.

A rectifying transformation is required to sense variations in texture contrast. Various theoretical and practical considerations have inclined researchers to suppose that this rectification is full-wave, rather than half-wave. In the studies reported here, observers are asked to judge which of two texture patches has higher texture variance. Textures are composed of small squares, with each square being painted with one of nine different luminances. Different texture variances are achieved by manipulating the histograms of the texture patches to be compared. When the nine luminances range linearly from 0 to 160 cd/m(2), the transformation mediating judgments of texture variance takes the form of a negative half-wave rectifier: texture variance judgments are determined exclusively by the frequencies of luminances below mean luminance in the textures being compared. However, when the nine luminances range linearly from 60 to 100 cd/m(2), two of three observers use a full-wave rectifying transformation in making texture variance judgments; the third observer continued to use a negative half-wave rectifier. The unexpectedly asymmetric roles played by low versus high luminances in texture variance judgments suggest that the off-center system may play a dominant role in human perception of texture contrast.