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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of mononuclear phagocytes with Cryptococcus neoformans was examined in vitro and in vivo using ultrastructural techniques. Immune serum roughens the surface of the yeast and in the first 2 hr, increases the number of organisms attaching to the macrophage surface, as well as the number of contacts between individual yeasts and the phagocyte. Contact is established by means of thin filopodia and cytoplasmic flaps. During the next few days the macrophages increase in size, and, by intimate apposition of their contiguous cell surfaces, a cellular barrier surrounds the now enclosed yeast. These events are accompanied by thinning of fungal capsule, degradation of the enclosed cryptococcus, and the formation of macrophage polykaryons. Electron cytochemical techniques for peroxidase reveal that these multinucleated cells are formed predominantly by the fusion of stimulated macrophages. Destruction of the enclosed yeast probably results from the secretion of various agents by the surrounding cells.
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PMID:An ultrastructural examination of the interaction between macrophages and Cryptococcus neoformans. 36 87

The correlation between glomerular immune deposition and histological alteration was studied in serial paraffin sections of kidney biopsy specimens from patients with IgA nephritis using the peroxidase-antiperoxidase (PAP) method. IgA deposition was detected in preserved glomerular extracellular matrix or in newly formed interposed matrix along the capillary loops (mesangial interposition). On the other hand, deposition of IgA was scanty or absent in the distorted extracellular matrix where severe exudative inflammation or extracapillary escape of exudates was occurring segmentally. Ultrastructurally such extracellular matricial destruction was expressed as splitting or thinning of the lamina densa, as well as mesangial edema, reticulation or mesangiolysis of the axial matrix. Therefore it appears that at least two types of change in the extracellular matrix are induced by IgA immune complexes in IgA nephritis; immunogenic deposition and destruction.
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PMID:Immunogenic deposition and destruction of glomerulus in IgA nephritis. 156 86

1. We applied morphological, pharmacological, electrophysiological, and computer simulation techniques to analyze the origin of impulse initiation in amphibian retinal ganglion cells. 2. Morphological studies of retinal ganglion cells in the mudpuppy (Necturus maculosus) and larval tiger salamander (Ambystoma tigrinum) were carried out with the use of either retrograde or intracellular labeling with horseradish peroxidase. These studies identified a characteristic thinning of the axon that begins after the initial segment of axon emerges from the ganglion cell soma or primary dendrite. Morphometric analysis of the thin segment revealed an average length of 74 microns with a standard deviation of 22 microns. For 20 conventionally placed ganglion cells, the length of the thin segment could not be correlated with soma size, initial segment diameter, or distance from the optic disk. There was also little or no correlation for seven displaced ganglion cells. The diameter of the thin segment was below reliable estimation by light microscopy. 3. We studied the possible significance of the thin axonal segment for ganglion cell impulse generation through a combination of electrophysiological recordings (intracellular and whole-cell recordings) together with computer modeling experiments. 4. Electrophysiological experiments are consistent with the idea that the thin segment and cell soma are less excitable than the initial segment region, which appears to be the principal site of initiation of the nerve impulse. The initial segment is that portion of the axon that is bounded by the soma (or proximal dendrite) at its origin and the thin segment at its distal end. 5. Computer simulations of impulse activation were carried out with the use of two different anatomic constraints: one class of simulations did not take into account the thin segment and assumed uniform cylinder conditions, whereas the other class of simulations included a model of the thin axonal segment. These comparative simulations indicate that the thin segment must contain a relatively high density of voltage-gated Na+ channels and support impulse traffic to account for physiological observations on orthodromic and antidromic impulse propagation. In addition, to match the physiological recordings, it is necessary for both the initial segment and the soma compartments to contain moderately high levels of Na+ channels. 6. Our physiological and simulation studies are consistent with the idea that the nerve impulse is normally initiated in the initial segment of axon and then spreads to activate a somatic impulse in the retrograde direction and the axonal impulse in the anterograde direction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Site of action potential initiation in amphibian retinal ganglion cells. 156 62

The development of the blood-cerebrospinal fluid (CSF) and cerebrospinal fluid-blood barriers, and the differentiation of the choroidal vessel wall, have been ultrastructurally investigated in the choroidal plexuses of the lateral ventricles of 10, 15, 18 and 21 day chicken embryos, fixed in normal conditions and also after intracardial and intraventricular injection of horseradish peroxidase. In all the analyzed developmental stages the choroidal epithelial cells seem able to endocytose and degradate, in their lysosomal apparatus, the tracer molecules reaching their ventricular and basolateral sides. The intravascularly injected horseradish peroxidase can enter the ventricular cavity by interepithelial route only at 10th incubation day, when the tight intercellular junctions are not formed everywhere, while a transepithelial transport is always hindered. The marker injected into the ventricular cavity reaches the subepithelial compartment and the blood stream, at 10th incubation day by interepithelial as well as transepithelial route and, successively, by transepithelial vesicular transport alone. The differentiation processes undergone by the choroidal blood vessels consist in a progressive thinning of the endothelial cells, appearance of pores, already numerous at 15th incubation day, and formation of the endothelial basement lamina, the final event in vessel wall maturation.
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PMID:The barrier systems in the choroidal plexuses of the chick embryo studied by means of horseradish peroxidase. 339 77

Neurons of the deep collicular layers were identified electrophysiologically, stained intracellularly with horseradish peroxidase and reconstructed from serial sections. Three neurons located in the stratum griseum intermedium were selected for detailed, light microscopic analyses. 7-10 dendritic stems arose from the polygonally shaped perikarya; they branch out in up to 8 successive bifurcations, giving rise to a mean of 9.1 tips per dendrite, or equivalently 78.7 tips per neuron. Dendrites extended up to 700 microns from soma, with tip diameters below 1 micron. Dendritic lengths were shown to be independent on branch order; mean branch length amounted to 72.3 microns, 96.3 microns and 99.4 microns. In each of the neurons, intermediate branches were significantly shorter than terminating branches. By excluding all of the end-branches, an inverse length-diameter relation could be demonstrated in each neuron to exist. Dendritic membrane surface area constituted more than 90% of the total soma-dendritic surface; dendritic-to-somatic surface area ratios were 9.8, 13.2 and 21.4, respectively. Measurements at 92 bifurcations of first to fourth order led to branch power n = 1.47 showing that the 3/2 power relationship is fulfilled on the average. All collicular neurons exhibited drastic arborizational taper due to disappearance of terminal branches, not to dendritic thinning within the tree. In spite of some differences among these deep collicular neurons in their general morphology, on many of the feature characterizing their dendritic trees they proved to be clearly similar confirming a previous description as single class of isodendritic, collicular neurons.
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PMID:Quantitative morphological analysis of deep superior colliculus neurons stained intracellularly with HRP in the cat. 357 61

A single injection of peroxidase-labelled Ricinus communis agglutinin (RCA-HRP) was given intracerebrally in 5-day old postnatal rats to determine its effects on neural tissues. The rats were sacrificed at various time intervals ranging from 1 hour to 8 weeks after the injection. 5 days after the injection, the lateral ventricle ipsilateral to the injection was progressively enlarged. The size of the ventricle continued to expand so that 10-15 days after the injection the ventricle on the contralateral side was also affected. In longer surviving rats, i.e 3-8 weeks after the injection, both the ventricles were extremely dilated resulting in the thinning of the cerebral cortex. Scanning electron microscopy of the dilated ventricles showed signs of disruption of the ependyma in some regions. A number of cells including macrophages, neurons, glioblasts, astrocytes and oligodendrocytes were present on the ependyma. Their identification was confirmed by scanning- and transmission electron microscopy. Transmission electron microscopy of the cerebral cortex subjacent to the dilated ventricles showed the presence of many degenerating neurons, 2-5 hours after the injection of RCA-HRP. The neurons displayed typical features of degeneration, i.e. displacement of nucleus, dilatation of cisternae of rough endoplasmic reticulum, and swelling and disintegration of mitochondria. In conclusion, following a single intracerebral injection of RCA-HRP, drastic neuronal degeneration was elicited near the site of injection and this resulted in the dilatation of the lateral ventricles similar to hydrocephalus.
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PMID:Induced hydrocephalus in postnatal rats following an intracerebral injection of ricin. 830 63

In the cat, areas 17 and 18 interconnect soon after birth. To test the hypothesis that the normal development of area 18 depends on interactions with area 17, unilateral lesions of area 17 were created in newborn kittens, and the animals allowed to mature. Horseradish peroxidase was then injected into both lateral geniculate nuclei. The major abnormalities of area 18 in the lesioned hemispheres were a thinning of specifically layers 2 and 3 and abnormally faint geniculocortical labelling of layer 4. Cell densities in layers 2 and 3 of the lesioned hemispheres were similar to or lower than normal. Neonatal destruction of area 17 therefore produced a selective loss of cells in layers 2 and 3 in area 18 (the layers that normally interconnect with area 17), and may have reduced thalamic innervation of layer 4.
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PMID:Lesions of area 17 in newborn kittens cause selective changes in the development of area 18. 874 51

The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.
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PMID:Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress. 936 53

Previous studies showed that uptake of the lectin conjugate, wheat germ agglutinin-horseradish peroxidase (WGA-HRP) by olfactory receptor cells results in a thinning of the olfactory epithelium (OE) and increased turnover of globose basal cells. To ascertain the cell-type lost as well as the time course and mechanism of the loss, the current study measured changes in the number of dendritic knobs, olfactory marker protein (OMP) expression and assessed TUNEL labeling as an indicator of apoptosis. Electron microscopic analysis of the number of dendritic knobs showed that the largest reduction occurred at 1 week after intranasal irrigation with WGA-HRP. This data in conjunction with decreased OMP staining provided evidence for a loss of mature receptor neurons. TUNEL labeling, especially in more superficial aspects of the OE, peaked at 18 hr after WGA-HRP application suggesting that the lectin-conjugate produced a rapid induction of apoptotic cell death that was complete by 3 days. Measurement of tyrosine hydroxylase (TH) activity in the olfactory bulb, a sensitive measure of deafferentation, showed that innervation reached a nadir at about 1 week and that reinnervation was complete by 4 weeks. These findings demonstrate that internalization of WGA-HRP by some receptor cells results in their death by apoptosis and a subsequent deafferentation of the olfactory bulb.
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PMID:Lectin-induced apoptosis of mature olfactory receptor cells. 1199 66

This study evaluated the involvement of hypophyseal-gonadal and hypophyseal-adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle-stimulating hormone, and estradiol along with sluggish ovarian activities of Delta(5),3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration.
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PMID:The involvement of hypophyseal-gonadal and hypophyseal-adrenal axes in arsenic-mediated ovarian and uterine toxicity: modulation by hCG. 2014 81


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