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Biomedical subjects

K G Go

Publications and source records attributed to K G Go.

17 recordsLinked to original sources
PubMed1992

Dextran-magnetite particles: contrast-enhanced MRI of blood-brain barrier disruption in a rat model.

Dextran-magnetite particles (DMP) were studied for their use as a MR contrast agent to visualize lesions with a blood-brain barrier (bbb) disruption. A freezing injury to the rat cerebral cortex was used as a model of bbb disruption. The biodistribution of iv-injected DMP was studied using atomic absorption spectrophotometry, electron microscopy, and MRI. One hour after injection, focal accumulation of the particles in capillary endothelial cells could be demonstrated in the freezing lesion. Despite the observation that the relaxivity of DMP in vivo appears to be less well pronounced than that in vitro, the MR imaging studies show that DMP can be used to visualize bbb disruption with adequate contrast.

Animals↗
PubMed1992

Specific MR imaging of human lymphocytes by monoclonal antibody-guided dextran-magnetite particles.

Human lymphocytes were labeled with biotinylated anti-lymphocyte-directed monoclonal antibodies, to which streptavidin and subsequently biotinylated dextran-magnetite particles were coupled. This labeling resulted in a strong and selective negative contrast enhancement of lymphocyte suspensions at 2.0 T, caused predominantly by the specific increase of R2 with a small but significant specific increase of R1. The R1 was found to decrease with increasing field strength. The immunolabeling procedure described here may be used for the selective signal depletion of target cells in MR imaging.

Antibodies, Monoclonal↗
PubMed1992

The pathogenesis of cerebral gliomatous cysts.

In this study, the authors have examined the mechanism of the formation of tumor cysts. Cyst fluid samples were obtained during surgery and by percutaneous aspiration from 22 patients with cystic cerebral gliomas. The concentration of protein was measured in the cyst fluid and blood plasma. Analysis of brain tumor cyst fluids revealed that plasma proteins constituted a major fraction (92%) of cyst fluid proteins; moreover, the protein fractions occurred in concentrations (relative to the plasma concentrations) that were around 50-fold of those in cerebrospinal fluid. This strongly indicates blood-brain barrier disruption. Evidence from computed tomographic and magnetic resonance imaging scans as well as from electron microscopy of tumor cyst walls suggests the transition of spongy edematous tissue in or around tumors into the contents of associated cysts. Pathophysiologically, blood-brain barrier breakdown is inherent to the occurrence of vasogenic brain edema. It is therefore plausible that the development of cysts is related to peritumoral vasogenic edema.

Albumins↗
PubMed1979

The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema.

Brain edema fluid was collected from cats with a freezing lesion in the left parietal cortex by the insertion into the brain of needles containing nylon wicks and connected to polyethylene tubes. The edema fluid samples which accumulated in the polyethylene tubes were regularly analyzed for Na+ and K+ content, colloid osmotic pressure, lactate dehydrogenase and creatine phosphokinase activity, and 99mTc-albumin radioactivity; the albumin tracer being introduced intravenously at the time of cold-injury. One series of cats received an intracerebral injection of ouabain solution, the control series an intracerebral injection of saline, at 100 min after the cold-injury. The ouabain injection was followed by an increase of K+ content, LDH and CPK activities but a decrease of Na+ concentration in the edema fluid, attributable to a concentration of solutes in the edema fluid as presumably water and Na+ were shifted into the cells and hence the extracellular space was reduced.

Animals↗
PubMed1979

Brain sodium uptake after choroid plexectomy.

When in a (control) series of rats brain sodium uptake (BSU) -- as calculated from estimated radioactivities of brain and blood following the injection of [24Na]sodium chloride 30 min and [22Na]sodium chloride one minute before killing -- was plotted against average arterial blood pressure of the animals during the 30 min survival period, a linear dependence of BSU on blood pressure was observed. In another series of animals, in which the choroid plexuses of the fourth and both lateral ventricles had been removed, the regression line showed the same slope, but a significantly lower intercept. On the other hand, a series of rats which had been subjected to a sham operation without removal of the choroid plexuses, showed a regression line not different from the control series. The results indicate that probably the blood pressure independent component of brain sodium uptake, as represented by the intercept of the regression line, for the greater part constitutes cerebrospinal fluid secretion by the choroid plexus.

Animals↗
PubMed1979

Composition of isolated edema fluid in cold-induced brain edema.

Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Albumins↗
PubMed1979

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema.

The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

Albumins↗
PubMed1978

Morphology and origin of arachnoid cysts. Scanning and transmission electron microscopy of three cases.

Three surgically removed primary arachnoidal cysts were studied with scanning electron microscopy (SEM) and two of the cases with transmission electron microscopy (TEM). The cells lining the cyst cavity had microvilli at the surface, true cilia were absent. In the cytoplasm multivesicular bodies, many pinocytotic vesicles, some large vacuoles and strands of tonofilaments were prominent features. The cells were interconnected by desmosome-like junctions and were separated from the surrounding tissue by a distinct but sometimes incomplete basal membrane. Based on these findings it is concluded that arachnoid cysts are derived from the outer arachnoid cells (subdural neurothelium), the formation of the cysts being attributabel to secretory capacity of the subdural neurothelium.

Adult↗
PubMed1977

Intrasacral meningocoele.

A case of an intrasacral meningocoele is described with typical radiological findings and obvious improvement after surgical treatment, but a somewhat unusual neurological picture.

Adult↗
PubMed1976

Experimental cerebral ischemia in Mongolian gerbils III. Behaviour of the blood-brain barrier.

The behavior of the BBB in cerebral ischemia was studied in symptom-positive Mongolian gerbils subjected to left common carotid artery occlusion using Evans Blue dye as indicator of BBB injury. The BBB damage was demonstrable grossly by the presence of areas of blue discoloration, and microscopically by the presence of a bright red fluorescent tracer, localized mostly in the neurons. The survey of various groups of animals revealed a direct relationship between the incidence and time of appearance of the BBB lesions and the duration of the ischemic occlusion. This relationship can be interpreted as another example of the previously described "maturation" phenomenon. A relatively late occurrence of the BBB injury in cerebral ischemia, at the time when the affected brain tissue shows severe, edematous histopathologic changes indicates that the brain edema, as the main complication of ischemia, could be regarded as being primarily of the cytotoxic type.

Animals↗
PubMed1976

Changes of ventricular ependyma and choroid plexus in experimental hydrocephalus, as observed by scanning electron microscopy.

Hydrocephalus was induced in rats by the injection of silicone oil or kaolin suspension into the cisterna magna. One to 5 weeks later the walls of the lateral ventricles were studied with the scanning electron microscope after killing the animals by perfusion fixation. In contrast to controls, the hydrocephalic animals killed 1 or 2 weeks after injection showed degeneration of ependymal cilia and infestation of the ependymal and choroid plexus surface with reactive cells, which presumably may be identified as Kolmer phagocytic cells by their ultrastructural features as studied by the transmission electron microscope. A coating of debris on the surface of the choroid plexus in the hydrocephalic animals possibly bears upon the ciliary degeneration with consequent deficiency of the clearing effect of ciliary movement. In the longer surviving hydrocephalic animals regeneration of cilia seemed to have occurred.

Animals↗
PubMed1975

The dependence of the blood to brain passage of radioactive sodium on blood pressure and temperature.

Brain sodium uptake (BSU) was calculated from estimated radioactivities of brain and blood, collected from rats which were given [24Na]sodium chloride 30 min and [22Na]sodium chloride 1 min before killing. The calculated BSU values, when plotted against the average blood pressure of the animal during the survival time of 30 min, showed a linear dependence of BSU on blood pressure. In another series of animals, in which in addition to variation of the blood pressure as in the former series, the brain was cooled to 15 degrees C, the resulting regression line showed the same slope, but a significantly lower intercept than at normal temperature. The results indicate the existence of a blood pressure-dependent component of sodium passage, reflecting the exchange of fluid at the blood-brain interface as governed by the Starling hypothesis, and an additional component which being temperature dependent, presumably constitutes an active transport mechanism.

Animals↗