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Biomedical subjects

A Eke

Publications and source records attributed to A Eke.

At least 19 recordsLinked to original sources

The modified Beer-Lambert law revisited.

The modified Beer-Lambert law (MBLL) is the basis of continuous-wave near-infrared tissue spectroscopy (cwNIRS). The differential form of MBLL (dMBLL) states that the change in light attenuation is proportional to the changes in the concentrations of tissue chromophores, mainly oxy- and deoxyhaemoglobin. If attenuation changes are measured at two or more wavelengths, concentration changes can be calculated. The dMBLL is based on two assumptions: (1) the absorption of the tissue changes homogeneously, and (2) the scattering loss is constant. It is known that absorption changes are usually inhomogeneous, and therefore dMBLL underestimates the changes in concentrations (partial volume effect) and every calculated value is influenced by the change in the concentration of other chromophores (cross-talk between chromophores). However, the error introduced by the second assumption (cross-talk of scattering changes) has not been assessed previously. An analytically treatable special case (semi-infinite, homogeneous medium, with optical properties of the cerebral cortex) is utilized here to estimate its order of magnitude. We show that the per cent change of the transport scattering coefficient and that of the absorption coefficient have an approximately equal effect on the changes of attenuation, and a 1% increase in scattering increases the estimated concentration changes by about 0.5 microM.

Absorption↗

Fractal characterization of complexity in temporal physiological signals.

This review first gives an overview on the concept of fractal geometry with definitions and explanations of the most fundamental properties of fractal structures and processes like self-similarity, power law scaling relationship, scale invariance, scaling range and fractal dimensions. Having laid down the grounds of the basics in terminology and mathematical formalism, the authors systematically introduce the concept and methods of monofractal time series analysis. They argue that fractal time series analysis cannot be done in a conscious, reliable manner without having a model capable of capturing the essential features of physiological signals with regard to their fractal analysis. They advocate the use of a simple, yet adequate, dichotomous model of fractional Gaussian noise (fGn) and fractional Brownian motion (fBm). They demonstrate the importance of incorporating a step of signal classification according to the fGn/fBm model prior to fractal analysis by showing that missing out on signal class can result in completely meaningless fractal estimates. Limitation and precision of various fractal tools are thoroughly described and discussed using results of numerical experiments on ideal monofractal signals. Steps of a reliable fractal analysis are explained. Finally, the main applications of fractal time series analysis in biomedical research are reviewed and critically evaluated.

Algorithms↗

Fractal branching pattern in the pial vasculature in the cat.

Arborization pattern was studied in pial vascular networks by treating them as fractals. Rather than applying elaborate taxonomy assembled from measures from individual vessel segments and bifurcations arranged in their branching order, the authors' approach captured the structural details at once in high-resolution digital images processed for the skeleton of the networks. The pial networks appear random and at the same time having structural elements similar to each other when viewed at different scales--a property known as self-similarity revealed by the geometry of fractals. Fractal (capacity) dimension, Dcap, was calculated to evaluate the network's spatial complexity by the box counting method (BCM) and its variant, the extended counting method (XCM). Box counting method and XCM were subject to numerical testing on ideal fractals of known D. The authors found that precision of these fractal methods depends on the fractal character (branching, nonbranching) of the structure they evaluate. Dcaps (group mean +/- SD) for the arterial and venous pial networks in the cat (n = 6) are 1.37 +/- 0.04, 1.37 +/- 0.02 by XCM, and 1.30 +/- 0.04, 1.31 +/- 0.03 by BCM, respectively. The arterial and venous systems thus appear to be developed according to the same fractal generation rule in the cat.

Animals↗

Physiological time series: distinguishing fractal noises from motions.

Many physiological signals appear fractal, in having self-similarity over a large range of their power spectral densities. They are analogous to one of two classes of discretely sampled pure fractal time signals, fractional Gaussian noise (fGn) or fractional Brownian motion (fBm). The fGn series are the successive differences between elements of a fBm series; they are stationary and are completely characterized by two parameters, sigma2, the variance, and H, the Hurst coefficient. Such efficient characterization of physiological signals is valuable since H defines the autocorrelation and the fractal dimension of the time series. Estimation of H from Fourier analysis is inaccurate, so more robust methods are needed. Dispersional analysis (Disp) is good for noise signals while bridge detrended scaled windowed variance analysis (bdSWV) is good for motion signals. Signals whose slopes of their power spectral densities lie near the border between fGn and fBm are difficult to classify. A new method using signal summation conversion (SSC), wherein an fGn is converted to an fBm or an fBm to a summed fBm and bdSWV then applied, greatly improves the classification and the reliability of H, the estimates of H, for the times series. Applying these methods to laser-Doppler blood cell perfusion signals obtained from the brain cortex of anesthetized rats gave H of 0.24+/-0.02 (SD, n=8) and defined the signal as a fractional Brownian motion. The implication is that the flow signal is the summation (motion) of a set of local velocities from neighboring vessels that are negatively correlated, as if induced by local resistance fluctuations.

Animals↗

Women's disclosure of HIV status: experiences of mistreatment and violence in an urban setting.

Women represent an increasing proportion of AIDS cases and anecdotal reports suggest some face substantial risks when others learn they are HIV-positive. The purpose of this paper is to describe women's fears and experiences regarding disclosure of their HIV status. Fifty HIV-positive women, ages 16-45 from urban teaching hospital outpatient clinics, were interviewed using an in-depth, qualitative interview. Eighty-six percent of the women were African American and 56% were current or former IVDU. At the time of the interview, 88% of the women had known their HIV status for a year or more. All but one woman had disclosed her HIV status to at least one person and 82% had disclosed to multiple people. Although two-thirds of the women had been afraid to disclose to others because of concerns about rejection, discrimination or violence, three-quarters of the sample reported only supportive and understanding responses to their disclosure. One-quarter of the sample reported negative consequences of disclosure, including rejection, abandonment, verbal abuse and physical assault. Disclosure-related violence was discussed by nine women (18%): two who feared violence were relieved to find a supportive response; four chose not to disclose their status because they feared violence; and three women were verbally or physically assaulted. Fear of mistreatment figured prominently in decisions about disclosure among this sample. That many women found supportive and understanding responses is encouraging. However, there were sufficient examples of negative consequences, including violence, to suggest individualized approaches to post-test counseling, enhanced support services for HIV-positive women, and public education to destigmatize HIV-disease.

Adolescent↗

A mathematical model of the intracerebral steal phenomenon in regional and focal ischaemia.

The objective of the present work was to mathematically estimate the extent and dynamics of intracerebral steal which may occur in response to cerebral vasodilation in regional and focal cerebral ischaemia. To this end, a spatially distributed mathematical model of regional cerebral blood flow (rCBF) was developed. The model contained a parallel system of intracerebral vascular resistances which were connected in series to a lumped extracerebral artery resistance and, for the focal ischaemia model, also a lumped pial collateral resistance. The rCBF was measured at 30 min of ischaemia in the following models: (1) bilateral carotid occlusion in spontaneously hypertensive rats (SHR), and (2) occlusion of the middle cerebral artery (MCA) in normotensive rats. The measured 3-dimensional rCBF data were used to set up the initial values of intracerebral resistance components. Cerebral vasodilation induced by inhalation of CO2 was simulated in the model by decreasing the values of both intracerebral and collateral resistance. Vascular responsiveness was specified to decrease with the ischaemic rCBF. In addition, a long term change in rCBF and resistance distribution was introduced to account for: (1) gradual rise in intracerebral resistance due to ischaemic oedema, and (2) adaptive decrease in collateral resistance. The following were predicted by the mathematical model. (1) At 60% maximum intracerebral dilatation a small intracerebral steal (5-10%) occurs at flow levels below 30-50 ml/100 g/min in both ischaemic models. (2) In focal ischaemia, the steal can be compensated by the 5% to 20% decrease in the collateral vascular resistance. (3) The rate of collateral adaptation overcomes the rate of intracerebral resistance rise and, therefore, eliminates the intracerebral steal after an adequately long period of time (on the order of a few hours). (4) An inverse steal effect can be demonstrated at the end of vasodilatation, provided that the time constant of collateral adaptation selected is longer (about 5:1) than the time constant of the intracerebral resistance rise. We conclude that the prediction of rCBF response to vasodilatation in cerebral ischaemia requires a knowledge of resting rCBF and of the response characteristics of both intracerebral and pial arterial segments.

Animals↗

Histologic assessment of neurons in rat models of cerebral ischemia.

We describe a method for typing neurons into four progressive stages of ischemic deterioration based on visual characterization of the nucleus in terms of its optical contrast, delineation along the nuclear-cytoplasmic interface, and its shape. Difficulty in assessing nuclear shape required the introduction of an angularity comparator chart to improve the investigator's accuracy. Three investigators typed neurons obtained from normal, ischemic, and ischemic-reperfused rat brains. Accuracy and reproducibility of the investigators' typing decisions with and without the angularity comparator charts were evaluated. The accuracy of subjective shape assessment was compared with objective digitizer measurements of the same. The angularity comparator charts reduced subjective shape classification error by two thirds, and group error (overall performance expressed by the coefficient of variance) decreased from 15.9% to 4.7% for Type I (normal cells), from 33.9% to 17.3% for Type II (cells with angular nuclei), from 15.5% to 14.1% for Type III (cells with smeared nuclei), and from 3.2% to 5.5% for Type IV (dead cells). Thus, Type I and IV neurons can be assessed at a higher reproducibility than the intermediate Types II and III. Our typing method can also be used to evaluate the effect of treatment regimes on ischemic neuronal damage.

Animals↗

Hematocrit changes in the extra- and intraparenchymal circulation of the feline brain cortex in the course of global cerebral ischemia.

Based on distinctly different hemodynamic behavior of erythrocytes and plasma affecting properties of the circulating blood in vivo, such as apparent viscosity, flow resistance, axial streaming of erythrocytes, plasma skimming, etc., hematocrit (Htc) can have an apparent impact on tissue perfusion. Hematocrit also shows a diameter dependent decrease along the extraparenchymal arterial vascular routes that levels off being markedly lower in the microcirculation than in the central arterial blood. It was postulated that the impact of Hct may become a critical aspect of the macro- and microcirculatory compensatory mechanisms under ischemic conditions, when excessive fluid shifts between the extra- and intravascular compartments can in fact alter both systemic and local Htc, and when a decreased perfusion pressure sets the stage for sluggish flow velocities at which orientation of erythrocytes in the plasma stream can abruptly change and impair the macro- and microcirculation alike. To test this hypothesis, systemic (Htcs), feed (Htcf) and local hematocrit (Htcl) were simultaneously monitored in anesthetized and mechanically ventilated cats from the abdominal aorta, a pial artery of 100 micra in diameter and 500-600 cerebrocortical microareas of 0.01 cubic mm each respectively, by a television densitometric method while global cerebral ischemia was induced and maintained by adjusting the systemic mean arterial blood pressure to 40-50 mmHg by controlled arterial hemorrhage. Global cerebral ischemia was terminated when cerebrocortical microcirculation collapsed or shed blood completely got reinfused to the animal. The data show that under control conditions Htcf is 44% of Htcs, while hemoconcentration in the tissue brings Htcl up to 67% of Htcs. Under ischemic conditions, in cases of short survival time, the extraparenchymal arterial hemoconcentration can not be sufficiently compensated by intraparenchymal hemodilution and the microcirculation collapses under the conditions of lowering or moderately rising local tissue hematocrit. In case of longer survival , the rate of extraparenchymal hemoconcentration is increasingly lower and therefore the intraparenchymal hemodilution becomes more effective and prolonged. Due to factors most likely pertinent to the tissue proper, microcirculation collapses under abruptly developing secondary tissue hemoconcentration. Since terminal Htcl was only slightly higher than that at the beginning of the ischemic episode, attention to other hemodynamic and rheological factors in the microcirculation--not directly influenced by Htc--have been turned to.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Classifying cells from light microscopic bit features by binary logic. Application to grade neuronal injury in cerebral ischemia.

Degradative cellular processes within neurons were analyzed and graded by a conceptually new approach that decoupled the process of subcellular feature analysis and grading, the latter being based on the severity of observed deterioration in subcellular features. Rather than evaluate the cell's histologic image in a panoramic manner, investigators were required to give simple yes-no decisions about the presence or absence of a specific pathologic feature (bit feature as opposed to panoramic analysis). Multiple elementary decisions create a binary representation of the cell image that can be easily handled and analyzed using computer techniques to generate all possible unique phenotypes of the scanned neuronal population. In the first application of this method, however, the number of possible phenotypes were reduced by imposed a priori logic on the separation scheme focusing on a single cellular structure (the nucleus) that was followed through the stages of structural decay. We experimentally validated four neuronal types of five theoretical possibilities when three nuclear bit features were used in typing. Grading of neuronal injury for groups of normal, ischemic, and ischemic and reperfused rats into two, three, and four categories are reported. The consistency at which the method can be implemented was assessed by calculating the mean and standard deviation of the reconciled typing decisions given by the four investigators. The group of the four investigators showed less than 2, 3, and 5% error when grading cells from control, ischemic, and ischemic-reperfused animals, respectively.

Animals↗