Perspective based on stereopsis and occlusion.

Perspective is usually considered a monocular pictorial cue, distinct from other cues such as occlusion and stereopsis. We cut across these distinctions by asking whether purely binocular (cyclopean) contours, created by stereoscopically shifting a region of homogeneous texture nearer or further than its surround, can act as a linear-perspective cue and whether the contours' ability to do this is influenced by their surface belongingness. We found that the left/right orientation of cyclopean trapezoids nearer than a surround strongly influenced perceived slant, showing that perspective constraints are applied to stereoscopically derived contours. Further regions, however; appeared as surfaces seen through a trapezoidal aperture. Because the aperture "owned" the trapezoidal contours, their orientation had little effect on perceived slant. We conclude that the application of perspective constraints depends critically on how contours are classified by stereo-specified occlusion relationships among surfaces and that perspective, stereopsis, and occlusion are not distinct processing systems.

Encouraging research in home care: learning from agency staff and family caregivers.

It is clear that research is an increasing role of managers and is crucial to the financial and clinical success of a home health agency. This article has described the important considerations and approaches managers must consider to integrate research effectively. By following one agency's involvement with a researcher on a project, strategies emerge that managers can use to integrate research with staff in everyday practice.

Understanding the aide/family caregiver relationship.

Family caregivers recognize the need for responsible, dependable home care services. When the services of the home care agency are required, it is often the aide who delivers the day-to-day care, whereas the home care nurse is responsible for providing coordination and supervision. The findings of this study provide the nurse with a better understanding of the relationship between home care aides and family caregivers.

Murine cytomegalovirus is present in both chronic active and latent states in persistently infected mice.

Cytomegalovirus induces serious disease in immunosuppressed individuals, often from an "activated" persistent infection. Whether the infection is chronically active or latent is unknown. Using murine cytomegalovirus (MCMV) in mice as a model system, we examined persistent infections in spleen, lung, and bone marrow of infected animals. At 28 days after infection, no virus could be recovered from any organs tested except salivary glands, and here, virus was cleared by 48 days. Virus could be retrieved at all times by cocultivation of spleen or lung with permissive cells. In addition, MCMV DNA was always present in spleen, lung, and bone marrow. After acute infection, RNA from the MCMV immediate early-1 (ie-1) gene was routinely found only in the lung. In spleen and bone marrow, only one sample from each organ examined at these times contained ie-1 RNA, and the RNA in these two samples was present at levels comparable to that found in acute infection. This suggests that the virus had reactivated. The ie-1 RNA found in the lung was present at a much lower RNA:DNA ratio than that found at early times. Taken together, these results indicate that persistent MCMV exists simultaneously in both chronic active and latent states.

Protozoa in subsurface sediments from sites contaminated with aviation gasoline or jet fuel.

Numbers of protozoa in the subsurface of aviation gasoline and jet fuel spill areas at a Coast Guard base at Traverse City, Mich., were determined. Boreholes were drilled in an uncontaminated location, in contaminated but untreated parts of the fuel plumes, and in the aviation gasoline source area undergoing H(2)O(2) biotreatment. Samples were taken from the unsaturated zone to depths slightly below the floating free product in the saturated zone. Protozoa were found to occur in elevated numbers in the unsaturated zone, where fuel vapors mixed with atmospheric oxygen, and below the layer of floating fuel, where uncontaminated groundwater came into contact with fuel. The same trends were noted in the biotreatment area, except that numbers of protozoa were higher. Numbers of protozoa in some contaminated areas equalled or exceeded those found in surface soil. The abundance of protozoa in the biotreatment area was high enough that it would be expected to significantly reduce the bacterial community that was degrading the fuel. Little reduction in hydraulic conductivity was observed, and no bacterial fouling of the aquifer was observed during biotreatment.

Colour inputs to random-dot stereopsis.

Recently it has been claimed by Livingstone and Hubel that, of three anatomically and functionally distinct visual channels (the magnocellular, parvocellular interblob, and blob channels), only the magnocellular channel is involved in the processing of stereoscopic depth. Since the magnocellular system shows little overt colour opponency, the reported loss of the ability to resolve random-dot stereograms defined only by colour contrast seems consistent with this view. However, Julesz observed that reversed-contrast stereograms could be fused if correlated colour information was added. In the present study, 'noise' (non-corresponding) pixels were injected into random-dot stereograms in order to increase fusion time. All six subjects tested were able to achieve stereopsis in less than three minutes when there was only correspondence in colour and not in luminance, and three when luminance contrast was completely reversed. This ability depends on information about the direction of colour contrast, not just the presence of chromatic borders. When luminance and chromatic contrast are defined in terms of signal-to-noise ratios at the photoreceptor mosaic, chromatic information plays at least as important a role in stereopsis as does luminance information, suggesting that the magnocellular channel is not uniquely involved.

Identification, transfer, and characterization of cloned herpes simplex virus invasiveness regions.

Following peripheral inoculation of experimental animals, herpes simplex virus type 2 (HSV-2) strains are more virulent than HSV-1 strains, and clinical studies suggest that they possess enhanced virulence in humans. One dramatic type-specific difference in virulence is observed following inoculation of the chorioallantoic membrane (CAM) of the chicken embryo: HSV-2, but not HSV-1, makes large pocks on the CAM, invades the mesoderm, generalizes in the embryo, and kills the chicken. These properties have been believed to be specific for HSV-2, and their molecular basis is unknown. We now report that an HSV-1 strain, ANG, behaves even more efficiently than HSV-2. In addition, we have transferred restriction fragments of ANG DNA to another HSV-1 strain, 17 syn+, conferring the CAM virulence phenotype on the normally CAM-avirulent 17 syn+. Like ANG, these recombinant viruses are 10(6)-fold more virulent (PFU/50%) lethal dose [LD50] ratio, less than or equal to 10(2)) than the parental 17 syn+ strain (PFU/LD50 ratio, greater than or equal to 10(8)). A molecularly cloned library of ANG DNA was used to identify two distinct regions containing the virulence functions. Transfer of sequences contained in either cloned ANG EcoRI fragment A (0.49 to 0.64 map units) or F (0.32 to 0.42 map units) DNA to 17 syn+ confers CAM virulence, whereas other cloned regions of the ANG genome do not. Using cloned DNA, we derived and plaque purified several virulent recombinant viruses with inserts from either the ANG EcoRI fragment A (INV-I) or F (INV-II) areas. In each instance, the transfer of the cloned INV-I or INV-II sequences enhanced virulence for the chicken embryo 10(6)-fold (PFU/LD50 ratio, less than or equal to 10(2]. In addition, the transfer of the cloned ANG EcoRI-F INV-II sequences resulted in a 10(3)-fold enhancement of neuroinvasiveness and virulence for mice. Following footpad inoculation, these recombinants kill mice with a PFU/LD50 ratio of approximately 10(3) (similar to HSV-2 strains) compared with 10(6) for 17 syn+. Thus, we have identified, cloned, and transferred two DNA regions from HSV-1 ANG which contain virulence genes (INV-I and INV-II) important in mesodermal invasiveness on the CAM and, in the case of INV-II, neuroinvasiveness in the mouse. In each instance, the recombinant HSV-1 viruses have attained enhanced virulence beyond that described for HSV-1 strains and similar to that seen with HSV-2.(ABSTRACT TRUNCATED AT 400 WORDS)

Cube copying after cerebral damage.

The capacity of patients with cerebral lesions to copy a picture of a cube, as opposed to a nonrepresentational figure of similar structural complexity, was examined. Patients with copying disability showed greater impairment for the cube than the noncube whereas patients without copying impairment and controls performed equally on the two figures. It was concluded that the copying-deficit patients had particular difficulty in drawing 3-dimensional figures and that the copying deficit was not simply one of formulating the sequence of steps necessary to produce a complex as opposed to a simple abstract form. The results suggest that copying-disability patients may experience particular difficulty in encoding the pictorial structure of a model which depicts a three-dimensional object. The occurrence of errors of intellectual realism in cube copying (which also occur in children's drawings) was noted and it was suggested that the patients were experiencing difficulty in perceptually isolating the picture structure from the picture content.

Prominence of the herpes simplex virus latency-associated transcript in trigeminal ganglia from seropositive humans.

Although herpes simplex virus type 1 (HSV-1) is known to reside latently in trigeminal ganglia between episodes of reactivation, the mechanisms involved in restricting the virus to this state are not understood. Using in situ nucleic acid hybridization methods, we show that there is HSV-encoded RNA in ganglion cells from 10 of 12 seropositive and zero of three seronegative patients studied at autopsy. Transcripts mapping to the region encoding the immediate-early polypeptide ICPO and the latency-associated transcript (LAT) were detected in the nuclei of these neurons. No other region of the HSV-1 genome was found to be expressed. When carefully defined probes were used to identify the transcripts, RNA corresponding to the LAT and, rarely, to ICPO was found. These results suggest that HSV-1 latency is an active process and that the LAT may be involved in regulating viral genetic expression.

RNA complementary to a herpesvirus alpha gene mRNA is prominent in latently infected neurons.

In initial attempts to define the molecular events responsible for the latent state of herpes simplex virus, in situ hybridization was utilized to search for virally encoded RNA transcripts in latently infected sensory neurons. The use of cloned probes representing the entire viral genome indicated that transcripts encoded within terminal repeats were present. When the alpha genes encoding ICP-0, ICP-4, and ICP-27 and the gamma 1 gene encoding VP-5 were employed, only RNA transcripts hybridizing to the ICP-0 probe were detected. In latently infected cells, the ICP-0--related transcripts were localized principally in the nucleus; this was not the case in acutely (productively) infected neurons or in neurons probed for RNA transcripts coding for actin. In Northern blotting experiments, an RNA of 2.6 kilobases was detected with the ICP-0 probe. When single-stranded DNAs from the ICP-0 region were used as probes, RNA from the strand complementary to that encoding ICP-0 messenger RNA (mRNA) was the major species detected. This RNA species may play a significant role in maintaining the latent infection.

A herpes simplex virus mutant is temperature sensitive for reactivation from the latent state: evidence for selective restriction in neuronal cells.

When the replicative defect in the HSV-1 temperature sensitive mutant tsI was repaired, the agent derived (RI-1) was found to possess an additional temperature sensitive lesion limiting its reactivation from the latent state. Thus, when spinal ganglia from latently infected mice were scored for reactivation by cocultivating them with indicator cells in vitro, significantly more were found to be positive at 31 degrees than at 38.5 degrees. To assess a possible relationship between reactivation and replication in neurons, the replication of RI-1 in murine C1300 neuroblastoma cells was studied. In these cells, RI-1 was severely restricted, and viral replication was delayed at 38.5 degrees. Serial passage of RI-1 in neuroblastoma cells at the restrictive temperature resulted in selection of an agent which gained both the capacity to replicate efficiently in neuroblastoma cells and reactivate from the latent state at 38.5 degrees. However, the replication pattern of this neuron adapted virus in mouse embryo fibroblasts remained unchanged from the parental RI-1. Taken together, these results indicate that RI-1 possesses a neuron specific temperature sensitive replicative lesion which is also manifest during reactivation from the latent state.

Functional and molecular analyses of the avirulent wild-type herpes simplex virus type 1 strain KOS.

It has been documented that KOS, a laboratory strain of herpes simplex virus type 1, is several orders of magnitude less neurovirulent than most other wild-type strains. Studies initiated to determine the functional nature of the block to neuroinvasiveness and to establish the genes involved have determined that, after footpad inoculation of mice, strain 17 syn+ induced neuropathologic signs (paralysis) at titers of 10(2) and yielded a PFU/50% lethal dose ratio of 10(4). In contrast, KOS was not lethal and did not induce paralysis at inoculation doses of 10(8) PFU. This reduced neurovirulence of KOS could not be explained by the lack of thymidine kinase activity, its inability to replicate in mouse cells maintained in culture at 38.5 degrees C, or its inefficient replication in nonneural tissues in vivo. Kinetic experiments tracing the virus through the nervous system after footpad inoculation showed that KOS was blocked at the level of the spinal ganglia. A cosmid library of strain 17 syn+ was utilized in recombination and in vivo selection experiments with strain KOS to establish the genomic region involved in 17 syn+ neuroinvasiveness. A cosmid clone containing the HindIII A fragment (0.25 to 0.53 map units) of strain 17 syn+ in mixed transfections with full-length KOS DNA yielded recombinants with enhanced neuroinvasiveness.

Microbial factors in contact lens fitting.

As contact lens practitioners, optometrists work in a nonsterile environment and on a nonsterile part of the human body. Our report describes 10 cases of eye infection related to contact lens wear. Practitioners need to be aware of the problems which can occur when a thoroughly sterilized contact lens is placed on an unsterile and biologically complex eye. We recommend taking swabs of the conjuctiva in all eyes where ocular inflammation is present. In those areas in which the professions of optometry and medicine meet, cooperation should exist. Improving our knowledge and skills in microbiology helps to facilitate such cooperation. Our experience has been most rewarding and interaction in this field with medical practitioners has been positive. The use of a high quality slitlamp is essential.

Anticonvulsant effects on the memory performance of epileptics.

The effects of different drugs on memory function in epileptic patients were examined. Patients had clinically normal cognitive function, above average IQs and infrequent seizures. Compared with pre-treatment evaluation, treatment with phenytoin, but not with carbamazepine or sodium valproate, resulted in impaired memory performance after three months of treatment. Switching patients previously treated with phenytoin to carbamazepine resulted in an improvement in memory performance compared with that of patients remaining on phenytoin. Switching patients from carbamazepine to sodium valproate did not result in any change in performance compared with that of those remaining on carbamazepine. The results of these experiments suggest that phenytoin, but not carbamazepine or sodium valproate, causes impaired memory performance. The nature of the memory dysfunction and its clinical implications are discussed.

Anticonvulsants, folic acid and memory dysfunction in epileptics.

The results of a survey of 116 epileptic patients treated by monotherapy with phenytoin, carbamazepine and sodium valproate are described. No significant correlations were found between memory performance and serum anticonvulsant levels. However, correlations were found between memory performance and levels of red cell folate. The hypothesis that phenytoin may impair memory performance through the reduction of folate is discussed.

Restricted replication of herpes simplex virus in spinal ganglia of resistant mice is accompanied by an early infiltration of immunoglobulin G-bearing cells.

In an attempt to define the nature of the difference in the susceptibility of C57BL/6 (resistant) and A/J (susceptible) mice to herpes simplex virus type 1, we initiated a study of virus progression through the nervous system. After inoculation of virus in a rear footpad, C57BL/6 mice were found to be more than 500-fold more resistant, but resistance did not extend to pseudorabies virus. In additional investigations, it was found that the virus was selectively restricted at the level of spinal ganglia in C57BL/6 mice. No intrinsic difference in the ability of this tissue from either mouse strain to replicate virus was found. However, by 4 days after infection, morphological investigations indicated that a mononuclear cell infiltrate was present surrounding infected neurons and satellite cells both earlier and in greater numbers in the ganglia of C57BL/6 mice. Immunohistochemical methods showed that most of these cells did not express Thy 1.2 antigen, but the vast majority bore immunoglobulin G. The mechanism by which these infiltrating cells could restrict virus spread is discussed.

Marek's disease as a model for the Landry--Guillain--Barré syndrome: latent viral infection in nonneuronal cells accompanied by specific immune responses to peripheral nerve and myelin.

In the chicken, Marek's disease virus (MDV) induces a demyelinating peripheral neuropathy that, early in the course of the disease, is histopathologically indistinguishable from that seen in the Landry--Guillain--Barré syndrome in man. A continuing role for a productive infection in the pathogenesis of this disease is unlikely, since neither MDV nor MDV antigens can be characteristically detected in nerves or spinal ganglia examined at necropsy. The authors investigated the possible role of a latent viral infection by explanting and maintaining in vitro the sciatic nerves and spinal ganglia from diseased birds. In these tissues, viral specific products were induced and detected by immunofluorescence and ultrastructural methods early after explanation in well-isolated Schwann cells, satellite cells, and lymphocytes. Later, virus was detected in fibroblasts, macrophages, and neoplastic lymphoblastoid cells. Neurons and myelinating Schwann cells, in contrast, did not replicate the agent. Specific cell-mediated and humoral immune responses to chicken peripheral nerve and peripheral nerve myelin were demonstrated early in the course of the disease. When considered relative to potential pathogenetic mechanisms, these results suggest that Marek's disease neuropathy is initiated by the establishment of a latent viral infection in neuronal supporting cells. A specific immune response to viral-induced antigens on these cells could, in turn, result in subsequent demyelination.

Marek's disease: a natural model for the Landry-Guillain-Barré syndrome.

The early lesions of Marek's disease in chickens are indistinguishable from those of the Landry-Guillain-Barré syndrome in human beings. Because of these similarities, and since the etiological agent (a herpesvirus) is known, Marek's disease can be meaningfully exploited as a model of the Landry-Guillain-Barré syndrome. Recent work in our laboratories has shown that the agent establishes latent infections in neuronal supporting cells and that affected birds mount cellular and humoral immunological reactions to peripheral nerve and myelin. Based on these findings, a working hypothesis for the pathogenesis of the disease is presented.