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Ultraviolet absorption cross sections of gas phase FNO3 and HOF have been measured over the wavelength range 180 to 400 nm at 295 K. The maximum photolysis lifetime for FNO3 in the stratosphere is calculated to be in the order of days, and for HOF in the order of hours.
The circadian rhythm in susceptibility to oxygen toxicity seizures was investigated by using six groups of 20 male Sprague-Dawley rats (101-196 gm.). The animals were given standard chow, exposed to standard diurnal conditions of light (0700-1900 hr) and dark (1900-0700 hr), and fasted for 15-16 hr prior to exposure to hyperbaric oxygen. The animals were placed in a previously oxygen flushed chamber and raised to 60 psi (gauge) oxygen at a rate of 3 psi/min. Time of exposure started with attainment of 60 psi. End point was first convulsion. The animals' weights were equally distributed within the groups, and the groups were defined by hour of exposure. Time of exposure in minutes prior to seizure was significantly longer in those exposed at 0700-0800 hr and 1000-1100 hr than in four other groups. There was no relationship between animals' weights and time of exposure to seizures. All R values were negative, and the highest R value was -035. These data suggest a definite circadian rhythm in susceptibility to oxygen toxicity seizures.
Albino Sprague-Dawley rats were exposed in a previously O2 flushed, CO2 free chamber. The exposure began with attainment of 60 psi (gauge) and the end point was the first generalized oxygen toxicity seizure. Animals were exposed to reversal diurnal conditions since weanlings until their sleep-wake cycles had completely reversed, and then divided into four groups of 20 based on the time of day exposed. The time of exposure to oxygen at high pressure prior to seizure was now significantly longer in the group exposed from 1900 to 2000 hr and a reversal of the circadian rhythm of oxygen toxicity seizure susceptibility was noted. Animals maintained on normal diurnal conditions were deprived of sleep on the day of exposure for the 12 hours prior to exposure at 1900 hr, while controls were allowed to sleep. There was no significant differences in the time prior to seizure between the deprived animals and the controls with an n = 40. Thus the inherent threshold in susceptibility to high-pressure oxygen seizures seems not to be a function of sleep itself, but of some biochemical/physiologic event which manifests a circadian rhythm.
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Over the last two decades, Mexico City, like many large industrial and populous urban areas, has developed a serious air pollution problem, especially during the winter months when there are frequent temperature inversions and weak winds. The deteriorating air quality is the result of several factors. The basin within which Mexico City lies in Mexico's center of political, administrative and economic activity, generating 34 percent of the gross domestic product and 42 percent of the industrial revenue, and supporting a population which is rapidly approaching the 20 million mark. The basin is surrounded by mountains on three sides which end up preventing rapid dispersal of pollutants. Emissions from the transportation fleet (more than 3 million vehicles) are one of the primary pollution sources, and most are uncontrolled. Catalytic converters are just now working their way into the fleet. The Mexico City Air Quality Research Initiative in an international collaboration project between the Los Alamos National Laboratory and the Mexican Petroleum Institute are dedicated to the investigation of the air quality problem in Mexico City. The main objective of the project is to identify and assess the cost and benefits of major options being proposed to improve the air quality. The project is organized into three main activity areas: (1) modeling and simulation; (2) characterization and measurements; and (3) strategic evaluation.
A lidar system based on ultraviolet (UV) laser induced fluorescence (LIF) was developed for the remote detection of atmospherically dispersed biological particles and chemical vapors. This UV fluorescence lidar has many potential applications for monitoring environmental pollution, industrial waste emission, agricultural insect control, illicit chemical processing, and military defense operations. The general goal of this work is to investigate the research issues associated with the long range detection and identification of chemicals, e.g. aromatic solvents and chemical precursors, and biological materials, e.g. bacillus thuringiensis (BT) and bacillus globiggi (BG). In the detection of biological particulates, we are particularly interested in extending the detection range of an existing solar-blind 248-nm lidar system. We are investigating the use of longer excitation laser wavelengths (i.e. lambda greater than 280-nm to have more favorable atmospheric light transmission characteristics) for improving detection range to better than 10 km. In the detection of chemical plumes, our main research objectives are to determine how accurately and sensitively a chemical plume can be located at range, and how well spectrally the chemical species can be measured to allow their identification.
There is a growing body of observational and theoretical evidence which suggests that local climate characteristics are associated with variations in the earth's surface. The link between surface variability and local-scale processes must be made if we are to improve our understanding of the feedback mechanisms involved in surface-atmosphere dynamics. However, to understand these interactions, the surface-atmosphere interface must be studied as a large-scale spatial system. Lidars are ideal tools to study the spatial properties of the atmosphere. The described techniques were developed for use with the Los Alamos Water Raman-Lidar, but are applicable to many other types of lidar. The methodology of the analysis of lidar data is summarized in order to determine meteorological parameters in the atmospheric boundary layer. The techniques are not exhaustive but are intended to show the depth and breadth of the information which can be obtained from lidars. Two methods for the computation of water-vapor fluxes were developed. The first uses the fact that the water vapor concentration in the vertical direction follows a logarithmic profile when corrected for atmospheric stability. The second method involves using inertial dissipation techniques in which lidar-derived spatial and temporal power spectra are used to determine the flux.
The Isotope Magnet Experiment (ISOMAX) a balloon-borne superconducting magnet spectrometer was designed to measure the isotopic composition of the light isotopes (3 less than or equal to Z less than or equal to 8) of the cosmic radiation up to 4 GeV nucleon (exp -1) with a mass resolution of better than 0.25 amu by using the velocity vs. rigidity technique. To achieve this stringent mass resolution ISOMAX was comprised of three major detector systems, a magnetic rigidity spectrometer with a precision drift chamber tracker in conjunction with a three-layer time-of-flight system and two silica-aerogel Cherenkov counters for the velocity determination. A special emphasis of the ISOMAX program was the accurate measurement of radioactive Be-10 with respect to its stable neighbor isotope Be-9, which provides important constraints on the age of cosmic rays in the Galaxy. ISOMAX had its first balloon flight on August 4-5, 1998, from Lynn Lake, Manitoba, Canada. Thirteen hours of data were recorded during this flight at a residual atmosphere of less than 5 g per square centimeter. The isotopic ratio at the top of the atmosphere for Be-10/Be-9 was measured to be 0.195 plus or minus 0.036 (statistical) plus or minus 0.039 (systematic) between 0.26 - 1.03GeV nucleon (exp -1) and 0.317 plus or minus 0.109 (statistical) plus or minus 0.042 (systematic) between 1.13 - 2.03GeV nucleon(exp -1). This is the first measurement of its kind above 1 GeV nucleon (exp -1). ISOMAX results tend to be higher than predictions from current propagation models.
The Isotope Magnet Experiment (ISOMAX), a balloon-borne superconducting magnet spectrometer, was designed to measure the isotopic composition of the light isotopes (3 les than or = Z less than or = 8) of cosmic radiation up to 4 GeV/nucleon with a mass resolution of better than 0.25 amu by using the velocity versus rigidity technique. To achieve this stringent mass resolution, ISOMAX was composed of three major detector systems: a magnetic rigidity spectrometer with a precision drift chamber tracker in conjunction with a three-layer time-of-flight system, and two silica-aerogel Cerenkov counters for velocity determination. A special emphasis of the ISOMAX program was the accurate measurement of radioactive Be-10 with respect to its stable neighbor isotope Be-9, which provides important constraints on the age of cosmic rays in the Galaxy. ISOMAX had its first balloon flight on 1998 August 4-5 from Lynn Lake, Manitoba, Canada. Thirteen hours of data were recorded during this flight at a residual atmosphere of less than 5 g/sq cm. The isotopic ratio at the top of the atmosphere for Be-10/Be-9 was measured to be 0.195 +/- 0.036 (statistical) +/- 0.039 (systematic) between 0.26 and 1.03 GeV/nucleon and 0.317 +/- 0.109(statistical) +/- 0.042(systematic) between 1.13 and 2.03 GeV/nucleon. This is the first measurement of its kind above l GeV/nucleon. ISOMAX results tend to be higher than predictions from current propagation models. In addition to the beryllium results, we report the isotopic ratios of neighboring lithium and boron in the energy range of the time-of-flight system (up to approx. 1 GeV/nucleon). The lithium and boron ratios agree well with existing data and model predictions at similar energies.
In recent years, the existence of visual variants of Alzheimer's disease characterized by atypical clinical presentation at onset has been increasingly recognized. In many of these cases post-mortem neuropathological assessment revealed that correlations could be established between clinical symptoms and the distribution of neurodegenerative lesions. We have analyzed a series of Alzheimer's disease patients presenting with prominent visual symptomatology as a cardinal sign of the disease. In these cases, a shift in the distribution of pathological lesions was observed such that the primary visual areas and certain visual association areas within the occipito-parieto-temporal junction and posterior cingulate cortex had very high densities of lesions, whereas the prefrontal cortex had fewer lesions than usually observed in Alzheimer's disease. Previous quantitative analyses have demonstrated that in Alzheimer's disease, primary sensory and motor cortical areas are less damaged than the multimodal association areas of the frontal and temporal lobes, as indicated by the laminar and regional distribution patterns of neurofibrillary tangles and senile plaques. The distribution of pathological lesions in the cerebral cortex of Alzheimer's disease cases with visual symptomatology revealed that specific visual association pathways were disrupted, whereas these particular connections are likely to be affected to a less severe degree in the more common form of Alzheimer's disease. These data suggest that in some cases with visual variants of Alzheimer's disease, the neurological symptomatology may be related to the loss of certain components of the cortical visual pathways, as reflected by the particular distribution of the neuropathological markers of the disease.
The perforant path, which consists of the projection from the layer II neurons of the entorhinal cortex to the outer molecular layer of the dentate gyrus, is a critical circuit involved in learning and memory formation. Accordingly, disturbances in this circuit may contribute to age-related cognitive deficits. In a previous study, we demonstrated a decrease in N-methyl-D-aspartate receptor subunit 1 immunofluorescence intensity in the outer molecular layer of aged macaque monkeys. In this study, we used the optical fractionator, a stereological method, to determine if a loss of layer II neurons occurred in the same animals in which the N-methyl-D-aspartate receptor subunit 1 alteration was observed. Our results revealed no significant differences in the number of layer II neurons between juvenile, young adult, and aged macaque monkeys. These results suggest that the circuit-specific decrease in N-methyl-D-aspartate receptor subunit 1 reported previously occurs in the absence of structural compromise of the perforant path, and thus may be linked to an age-related change in the physiological properties of this circuit.
Previous immunohistochemical studies combined with retrograde tracing in macaque monkeys have demonstrated that corticocortical projections can be differentiated by their content of neurofilament protein. The present study analyzed the distribution of nonphosphorylated neurofilament protein in callosally projecting neurons located at the V1/V2 border. All of the retrogradely labeled neurons were located in layer III at the V1/V2 border and at an immediately adjacent zone of area V2. A quantitative analysis showed that the vast majority (almost 95%) of these interhemispheric projection neurons contain neurofilament protein immunoreactivity. This observation differs from data obtained in other sets of callosal connections, including homotypical interhemispheric projections in the prefrontal, temporal, and parietal association cortices, that were found to contain uniformly low proportions of neurofilament protein-immunoreactive neurons. Comparably, highly variable proportions of neurofilament protein-containing neurons have been reported in intrahemispheric corticocortical pathways, including feedforward and feedback visual connections. These results indicate that neurofilament protein is a prominent neurochemical feature that identifies a particular population of interhemispheric projection neurons at the V1/V2 border and suggest that this biochemical attribute may be critical for the function of this subset of callosal neurons.
Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.
Previous studies of the primate cerebral cortex have shown that neurofilament protein is present in pyramidal neuron subpopulations displaying specific regional and laminar distribution patterns. In order to characterize further the neurochemical phenotype of the neurons furnishing feedforward and feedback pathways in the visual cortex of the macaque monkey, we performed an analysis of the distribution of neurofilament protein in corticocortical projection neurons in areas V1, V2, V3, V3A, V4, and MT. Injections of the retrogradely transported dyes Fast Blue and Diamidino Yellow were placed within areas V4 and MT, or in areas V1 and V2, in 14 adult rhesus monkeys, and the brains of these animals were processed for immunohistochemistry with an antibody to nonphosphorylated epitopes of the medium and heavy molecular weight subunits of the neurofilament protein. Overall, there was a higher proportion of neurons projecting from areas V1, V2, V3, and V3A to area MT that were neurofilament protein-immunoreactive (57-100%), than to area V4 (25-36%). In contrast, feedback projections from areas MT, V4, and V3 exhibited a more consistent proportion of neurofilament protein-containing neurons (70-80%), regardless of their target areas (V1 or V2). In addition, the vast majority of feedback neurons projecting to areas V1 and V2 were located in layers V and VI in areas V4 and MT, while they were observed in both supragranular and infragranular layers in area V3. The laminar distribution of feedforward projecting neurons was heterogeneous. In area V1, Meynert and layer IVB cells were found to project to area MT, while neurons projecting to area V4 were particularly dense in layer III within the foveal representation. In area V2, almost all neurons projecting to areas MT or V4 were located in layer III, whereas they were found in both layers II-III and V-VI in areas V3 and V3A. These results suggest that neurofilament protein identifies particular subpopulations of corticocortically projecting neurons with distinct regional and laminar distribution in the monkey visual system. It is possible that the preferential distribution of neurofilament protein within feedforward connections to area MT and all feedback projections is related to other distinctive properties of these corticocortical projection neurons.
The primate cingulate gyrus contains multiple cortical areas that can be distinguished by several neurochemical features, including the distribution of neurofilament protein-enriched pyramidal neurons. In addition, connectivity and functional properties indicate that there are multiple motor areas in the cortex lining the cingulate sulcus. These motor areas were targeted for analysis of potential interactions among regional specialization, connectivity, and cellular characteristics such as neurochemical profile and morphology. Specifically, intracortical injections of retrogradely transported dyes and intracellular injection were combined with immunocytochemistry to investigate neurons projecting from the cingulate motor areas to the putative forelimb region of the primary motor cortex, area M1. Two separate groups of neurons projecting to area M1 emanated from the cingulate sulcus, one anterior and one posterior, both of which furnished commissural and ipsilateral connections with area M1. The primary difference between the two populations was laminar origin, with the anterior projection originating largely in deep layers, and the posterior projection taking origin equally in superficial and deep layers. With regard to cellular morphology, the anterior projection exhibited more morphologic diversity than the posterior projection. Commissural projections from both anterior and posterior fields originated largely in layer VI. Neurofilament protein distribution was a reliable tool for localizing the two projections and for discriminating between them. Comparable proportions of the two sets of projection neurons contained neurofilament protein, although the density and distribution of the total population of neurofilament protein-enriched neurons was very different in the two subareas of origin. Within a projection, the participating neurons exhibited a high degree of morphologic heterogeneity, and no correlation was observed between somatodendritic morphology and neurofilament protein content. Thus, although the neurons that provide the anterior and posterior cingulate motor projections to area M1 differ morphologically and in laminar origin, their neurochemical profiles are similar with respect to neurofilament protein. This suggests that neurochemical phenotype may be a more important unifying feature for corticocortical projections than morphology.
The neurochemical characteristics of the neuronal subsets that furnish different types of corticocortical connections have been only partially determined. In recent years, several cytoskeletal proteins have emerged as reliable markers to distinguish subsets of pyramidal neurons in the cerebral cortex of primates. In particular, previous studies using an antibody to nonphosphorylated neurofilament protein (SMI-32) have revealed a consistent degree of regional and laminar specificity in the distribution of a subpopulation of pyramidal cells in the primate cerebral cortex. The density of neurofilament protein-immunoreactive neurons was shown to vary across corticocortical pathways in macaque monkeys. In the present study, we have used the antibody SMI-32 to examine further and to quantify the distribution of a subset of corticocortically projecting neurons in a series of long ipsilateral corticocortical pathways in comparison to short corticocortical, commissural, and limbic connections. The results demonstrate that the long association pathways interconnecting the frontal, parietal, and temporal neocortex have a high representation of neurofilament protein-enriched pyramidal neurons (45-90%), whereas short corticocortical, callosal, and limbic pathways are characterized by much lower numbers of such neurons (4-35%). These data suggest that different types of corticocortical connections have differential representation of highly specific neuronal subsets that share common neurochemical characteristics, thereby determining regional and laminar cortical patterns of morphological and molecular heterogeneity. These differences in neuronal neurochemical phenotype among corticocortical circuits may have considerable influence on cortical processing and may be directly related to the type of integrative function subserved by each cortical pathway. Finally, it is worth noting that neurofilament protein-immunoreactive neurons are dramatically affected in the course of Alzheimer's disease. The present results support the hypothesis that neurofilament protein may be crucially linked to the development of selective neuronal vulnerability and subsequent disruption of corticocortical pathways that lead to the severe impairment of cognitive function commonly observed in age-related dementing disorders.
The human anterior cingulate cortex is distinguished by the presence of an unusual cell type, a large spindle neuron in layer Vb. This cell has been noted numerous times in the historical literature but has not been studied with modern neuroanatomic techniques. For instance, details regarding the neuronal class to which these cells belong and regarding their precise distribution along both ventrodorsal and anteroposterior axes of the cingulate gyrus are still lacking. In the present study, morphological features and the anatomic distribution of this cell type were studied using computer-assisted mapping and immunocytochemical techniques. Spindle neurons are restricted to the subfields of the anterior cingulate cortex (Brodmann's area 24), exhibiting a greater density in anterior portions of this area than in posterior portions, and tapering off in the transition zone between anterior and posterior cingulate cortex. Furthermore, a majority of the spindle cells at any level is located in subarea 24b on the gyral surface. Immunocytochemical analysis revealed that the neurofilament protein triple was present in a large percentage of these neurons and that they did not contain calcium-binding proteins. Injections of the carbocyanine dye DiI into the cingulum bundle revealed that these cells are projection neurons. Finally, spindle cells were consistently affected in Alzheimer's disease cases, with an overall loss of about 60%. Taken together, these observations indicate that the spindle cells of the human cingulate cortex represent a morphological subpopulation of pyramidal neurons whose restricted distribution may be associated with functionally distinct areas.
Visual function in monkeys is subserved at the cortical level by a large number of areas defined by their specific physiological properties and connectivity patterns. For most of these cortical fields, a precise index of their degree of anatomical specialization has not yet been defined, although many regional patterns have been described using Nissl or myelin stains. In the present study, an attempt has been made to elucidate the regional characteristics, and to varying degrees boundaries, of several visual cortical areas in the macaque monkey using an antibody to neurofilament protein (SMI32). This antibody labels a subset of pyramidal neurons with highly specific regional and laminar distribution patterns in the cerebral cortex. Based on the staining patterns and regional quantitative analysis, as many as 28 cortical fields were reliably identified. Each field had a homogeneous distribution of labeled neurons, except area V1, where increases in layer IVB cell and in Meynert cell counts paralleled the increase in the degree of eccentricity in the visual field representation. Within the occipitotemporal pathway, areas V3 and V4 and fields in the inferior temporal cortex were characterized by a distinct population of neurofilament-rich neurons in layers II-IIIa, whereas areas located in the parietal cortex and part of the occipitoparietal pathway had a consistent population of large labeled neurons in layer Va. The mediotemporal areas MT and MST displayed a distinct population of densely labeled neurons in layer VI. Quantitative analysis of the laminar distribution of the labeled neurons demonstrated that the visual cortical areas could be grouped in four hierarchical levels based on the ratio of neuron counts between infragranular and supragranular layers, with the first (areas V1, V2, V3, and V3A) and third (temporal and parietal regions) levels characterized by low ratios and the second (areas MT, MST, and V4) and fourth (frontal regions) levels characterized by high to very high ratios. Such density trends may correspond to differential representation of corticocortically (and corticosubcortically) projecting neurons at several functional steps in the integration of the visual stimuli. In this context, it is possible that neurofilament protein is crucial for the unique capacity of certain subsets of neurons to perform the highly precise mapping functions of the monkey visual system.