Distribution Of Cell Loss Research Articles

Performance evaluation of discrete event systems involving Henstock-Kurzweil integral

This paper presents a study on the performance of flexible manufacturing systems (FMSs), by using discrete event system (DES) models, considering resource losses modelled by a parameter entitled coverage factor. We conclude that the resources cell loss distribution between the tasks of a FSM is a real function that cannot be integrated, in order to calculate its primitive, in the classical sense of Riemann or Lebesgue, but only in the sense of Henstock-Kurzweil integral. Our result allows one to study more general processes where highly oscillatory functions occur. The method used to deduce the function describing the resources cell loss distribution is compared with a classical method related in the literature, respectively rational interpolants. An example has been constructed to emphasize what we believe to be, new approaches.

Topographic distribution of seizure onset and hippocampal atrophy: Relationship between MRI and depth EEG

Medial temporal lobe epilepsy (MTLE) is associated with hippocampal cell loss and organization of the dentate gyrus. Some studies suggest a correlation between the topographic distribution of cell loss and site of epileptogenesis. We studied the relationship between the site of ictal onset with the presence of segmental atrophy in patients with non-lesional MTLE using magnetic resonance imaging (MRI) and depth EEG. Ictal recordings were obtained from 27 patients with longitudinal hippocampal depth electrodes and variable combinations of subdural strips sampling medial temporal structures. The location of the depth electrode contacts was correlated with anatomical landmarks. Seizures were analyzed for the distribution of onset along the long axis of the hippocampus. MRI analysis were performed to detect segmental atrophy. Outcome was assessed 1 year or more following anterior temporal lobectomy. Twenty-five patients had unilateral, and two had bilateral, hippocampal atrophy. One hundred and forty-seven seizures were reviewed: 21 showed focal onset and 126 showed regional onset. Ictal onset involved the amygdala and anterior half of the hippocampus in 80% of the seizures while only 40% of patients had atrophy of these segments. Most patients had excellent outcome. In patients with MTLE the primary area of epileptogenesis does not parallel the hippocampal segments with the greatest degree of volume loss.

Steel's potential doubling time and its estimation in cell populations affected by nonuniform cell loss.

The in vivo infusion of the thymidine analogue bromodeoxyuridine (BrdUrd). followed by delayed biopsy and bivariate DNA-BrdUrd flow cytometry, makes it possible to estimate Steel's potential doubling time (Tpot) of human tumors. In the present paper, the expression of Steel's Tpot for a rather general cell population model, in which the distribution of cell loss is assumed to be nonuniform, is derived in terms of the model parameters. We show that Steel's Tpot of a population can be markedly different for the doubling time that would be exhibited by the population in the absence of cell loss. These doubling times, on the contrary, are equal when loss is uniform. Moreover, we studied the influence of modes of cell loss different from the uniform random loss on the estimation of Tpot by using the labeling index or the nu-function, quantities that can be determined from the bivariate DNA-BrdUrd distribution.

The N-methyl-D-aspartate antagonist, MK-801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats

The neuroprotective effects of dizocilipine maleate (MK-801), a noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) receptor/channel, were tested in the 4-vessel occlusion rat model of forebrain ischemia. Adult Wistar rats, treated intraperitoneally with MK-801 or saline using several different treatment paradigms were subjected to 5 (n = 208) or 15 (n = 62) min of severe, transient forebrain ischemia. In saline-treated animals, 15 min of ischemia (n = 13) produced extensive and consistent loss of pyramidal neurons in the CA1 zone of hippocampus. The degree and distribution of cell loss were not reduced by single dose preischemic administration of MK-801 at 1 (n = 7), 2.5 (n = 4), or 5 mg/kg (n = 8). In other animals subjected to 15 min of forebrain ischemia, multiple doses of MK-801 (5, 2.5, and 2.5 mg/kg) given immediately and at approximately 8 and 20 hr after cerebral reperfusion (n = 5) did not alter CA1 injury compared to saline-treated controls (n = 5). Five minutes of forebrain ischemia in saline-treated animals, (n = 82) resulted in significantly fewer (p less than 0.001) dead CA1 pyramidal cells and a greater variance compared to animals subjected to 15 min of ischemia. Power analysis of the preliminary saline-treated animals subjected to 5 min of ischemia (n = 22) indicated that 60 animals per group were necessary to detect a 15% difference between MK-801 and vehicle-treated groups. Multidose treatment with MK-801 (1 mg/kg) given 1 hr prior to 5 min of ischemia (n = 60) and again at approximately 8 and 16 hr after recirculation failed to attenuate hippocampal injury.(ABSTRACT TRUNCATED AT 250 WORDS)

A histometrical and comparative study on Purkinje cell loss and olivary nucleus cell loss in multiple system atrophy

We examined pathologically 21 cases of multiple system atrophy (MSA). Density of Purkinje cell in 16 cases and of olivary nucleus cell in 20 cases was quantitatively measured, and their distribution as well as degree were studied. Contrary to the findings of previous reports, Purkinje cell loss was more pronounced in the vermis than in the hemispheres. Olivary nucleus cell loss was more outstunding in the accessory nucleus than in the inferior nucleus. A topographical characteristic of cell degeneration exists between the Purkinje layer and the olivary nucleus. Significant sparing of the nodulus apparently related to that of the vestibular system was found. While the common distribution of cell loss was seen, its degree varied considerably case by case. The degree was related to both duration of illness and, to some extent, clinical subtypes of MSA.

AGEING AND PARKINSON'S DISEASE: SUBSTANTIA NIGRA REGIONAL SELECTIVITY

The micro-architecture of the substantia nigra was studied in control cases of varying age and patients with parkinsonism. A single 7 mu section stained with haematoxylin and eosin was examined at a specific level within the caudal nigra using strict criteria. The pars compacta was divided into a ventral and a dorsal tier, and each tier was further subdivided into 3 regions. In 36 control cases there was a linear fallout of pigmented neurons with advancing age in the pars compacta of the caudal substantia nigra at a rate of 4.7% per decade. Regionally, the lateral ventral tier was relatively spared (2.1% loss per decade) compared with the medial ventral tier (5.4%) and the dorsal tier (6.9%). In 20 Parkinson's disease (PD) cases of varying disease duration there was an exponential loss of pigmented neurons with a 45% loss in the first decade. Regionally, the pattern was opposite to ageing. Loss was greatest in the lateral ventral tier (average loss 91%) followed by the medial ventral tier (71%) and the dorsal tier (56%). The presymptomatic phase of PD from the onset of neuronal loss was estimated to be about 5 yrs. This phase is represented by incidental Lewy body cases: individuals who die without clinical signs of PD or dementia, but who are found to have Lewy bodies at post-mortem. In 7 cases cell loss was confined to the lateral ventral tier (average loss 52%) congruent with the lateral ventral selectivity of symptomatic PD. It was calculated that at the onset of symptoms there was a 68% cell loss in the lateral ventral tier and a 48% loss in the caudal nigra as a whole. The regional selectivity of PD is relatively specific. In 15 cases of striatonigral degeneration the distribution of cell loss was similar, but the loss in the dorsal tier was greater than PD by 21%. In 14 cases of Steele-Richardson-Olszewski syndrome (SRO) there was no predilection for the lateral ventral tier, but a tendency to involve the medial nigra and spare the lateral. These findings suggest that age-related attrition of pigmented nigral cells is not an important factor in the pathogenesis of PD.