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The authors aim to present the problematics of hemorrhoid treatment using the Barron ligature semiinvasive method, to healthcare professionals.

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The efficiency of the sorbent prepared by immobilization of [Iron(II)hexacyanoferrate(II)] on clinoptilolite--marked as ZEOFe--in reduction of the radiocaesium Cs-137 has been in vivo investigated in sheep. It was found that an application of this modified clinoptilolite affected both primary and secondary resorption of Cs-137 also by interrupting the enteral cycle of radiocaesium in sheep. It was proved that ZEOFe accelerated approx. twice the excretion of Cs-137 from sheep's body. The whole effect resulted in 15 to 50 times lowering of the equilibrium concentration of radiocaesium in the case of constant intake of the contaminated feed and simultaneous application of 50 grams of ZEOFe daily. The actual reduction depends mainly on the way of administration. The reduction of Cs-137 by non-modified clinoptilolite--ZEO--has been investigated, too. More than 10x lower sorption efficiency has been observed in comparison with ZEOFe.

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The uptake of radiocesium Cs-137 in rabbit's muscle and its clearance were studied following the 24 days long ingestion of hay naturally contaminated as a consequence of the Chernobyl accident. The average radioactivity of hay was 2,294 +/- 345 Bq/kg and the daily intake was 0.5 kg. It was found that after 20 days of ingestion the muscle radionuclide concentration equilibrated with that of the feed. The transfer coefficient Tf describing the fraction of the daily intake of Cs-137 found in a kilogram of rabbit's muscle was calculated: Tf = 0.29 +/- 0.15 d/kg. The biological Cs-137 clearance rate (after finishing the feeding with contaminated diet) was found to be ruled by two biological half-lives: Tb1 = 1.5 days and Tb2 = 66 days and fitting the following retention equation: At = 0.66.e-0.46.t + 0.34.e-0.01.t It means that 5 days after removing the animals from contaminated diet the amount of Cs-137 can be expected as 30% of the initial one.

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The efficiency of an active substance (AL) prepared in our laboratory as a composite sorbent on the basis of hexacyanoferrates (II) bound on pearl cellulose, in affecting the radiocesium (Cs-137) retention in white miniature pigs was investigated. The function of the composite sorbent in dependence on the way of administration, i.e. its effect on a decrease of primary resorption and its ability to interrupt the enteral cycle was studied, too. The efficiency of stable cesium administration in the form of CsCl in the same process was also determined. It was proved that AL accelerated significantly the excretion through its effect both on primary resorption causing an approx. 11-fold reduction of resorption when administered simultaneously with radiocesium and on the enteral cycle, causing an approx. 3.5-fold increase of excretion of Cs-137 when administered daily. Thus the composite sorbent (AL) administered at long-term along with contaminated feed reduced the equilibrium concentration of radiocesium in meat 30-40 times. This might be of great importance in the time of nuclear emergencies. On the other hand, administration of non-active Cs at a level up to 1 mg Cs/1 kg of liveweight had no significant effect on Cs-137 elimination.

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An investigation of 25,000 samples of foodstuffs and feedstuffs in Czechoslovakia, contaminated by fall-out cesium after the accident in the Chernobyl nuclear power plant, performed from May 5, 1986 to March 31, 1988, revealed that both the values of cesium transfer-factors in food--animal tissues--milk transitions and the values of biological half-life of cesium are functions of internal and external conditions of contamination. Organism individuality as the main internal condition causes the variance of about +/- 50% of the mean value of the respective transfer-factor. Through the external conditions, mainly the environmental contamination level, type of ingested food and time of ingestion, the mean values of transfer-factors are influenced up to 500%, e.g. to the value of 0.5. But this value converges with growing up contamination of food and environment to the limit of 0.3. The first two to three biological half-lives after the last ingestion of contaminated food are up to ten-times shorter than those at stabilized state.

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The effects of pickle-curing on a decrease in the cesium-nuclides amount in red-deer meat were investigated. This meat was contaminated through ingestion of natural feed in seasons after the fall-out from Chernobyl accident. Two pickles were studied: vinegar solution and the same one with added vegetables and spices. The pickle curing was carried out at temperatures of 5 degrees C and 11 degrees C after cutting the meat into little pieces of about 1.5 cm. Adecrease in cesium activity was measured by means of gamma-spectrometry at given time intervals after the process was started. It was proved that the efficiency of this process is mostly influenced by replacement of the pickle solution and by the duration of the process. A decrease in the cesium activity of about 80% was achieved without the change of the pickle after seven hours of curing. But after the same time and one pickle solution change, the activity decrease reached more than 90%. No important influence of added vegetables and spices into the pickle nor of the temperature between 5 degrees C and 11 degrees C was observed.

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A radioactive contamination monitoring system of the Czechoslovak Federal Ministry of Agriculture and Food is described, including measuring and calibration methods and the monitoring results. Cesium contamination higher than the international derived intervention level was found only in game. The reasons were as follows: uncultivated green fields, forest herbage and needle-leaves are sufficient sources of game contamination; there exist evident differences between continuous ingestion of contaminated or mixed feed with respect to the cesium contamination of tissues.

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Red cells coated with IgG globulin were bound firmly to human mononuclear cells and formed rosettes. Rosette formation occurred when red cells were coated with IgG attached either immunologically (anti-D, anti-penicillin, or Donath-Landsteiner antibodies) or nonimmunologically with chromic chloride; no attachment was observed with cells coated with albumin. Rosette formation was blocked by pretreatment of white cells with sulfhydryl-binding reagents. Metabolic inhibitors did not prevent red cell adherence. White cells of other primates demonstrated a high degree of species specificity. Ultrastructural studies showed that the predominant leukocytes involved in rosette formation were monocytes, but some cells with characteristics of lymphocytes also formed rosettes. Considerable interdigitation of cell surfaces occurred at attachment sites and bound red cells appeared deformed. Thus, these studies confirm the presence of specific surface receptors for IgG on human monocytes and suggest that such receptors may provide a mechanism by which large numbers of red cells are eventually destroyed.

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Studies were carried out in order to characterize the specificity of IgG sub-classes and IgG fragments for rosette formation using red cells and human mononuclear cells. Rosette formation of red cells coated with anti-D was inhibited by free IgG(1) and IgG(3); less inhibition occurred with IgG(2) and IgG(4). Red cells specifically coated with IgG(1) and IgG(3) by chromic chloride were bound to monocytes. Rosette inhibition of anti-D-coated red cells occurred with free Fc fragment of IgG globulin, and only partly with F(ab')(2). Inhibitory capacity of Fc fragments of IgG and gamma(1) heavy chain from heavy chain disease was reversed by the cleavage of disulfide bonds. No inhibition was noted with Fab, or with pepsin components II, III, or IV. These studies indicated that the mononuclear receptor was specific for IgG(1) and IgG(3). The peptide portion of IgG globulin which attached to the mononuclear cell appeared to reside in the N-terminal portion of the Fc fragment and also appeared to require the integrity of the inter-heavy chain disulfide bond. A specific receptor for C3 was not confirmed.

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In a patient with increased susceptibility to infection, lowered serum C3 concentration, and continuously circulating C3b, it was shown that purified (125)I-labeled C3 was converted to labeled C3b shortly after intravenous administration. The fractional catabolic rate of C3 was approximately five times normal at 10% of the plasma pool per hr. The synthesis rate and pool distribution of C3 were normal. Despite this evidence of C3 instability in vivo, no accelerated inactivation of C3 was found in vitro. Similarly, no free proteolytic activity could be detected in the patient's serum, and serum concentrations of known protease inhibitors were normal.Complement-mediated functions, which were markedly deficient in the patient's serum, could be restored partially or completely by the addition of a 5-6S heat-labile beta pseudoglobulin from normal serum. The C3 proinactivator, which has these physicochemical characteristics, was also shown to be either absent or nonfunctional in the patient's serum. An unidentified 6S beta pseudoglobulin to which a monospecific antiserum was available was not detectable in the patient's serum. This last protein appeared not to be a complement component, nor was it the C3 inactivator or proinactivator. Finally, the substance or substances necessary for the conversion of C3b to C3c were missing from the patient's serum. The administration of 500 ml of normal plasma to the patient corrected all of his abnormalities partially or completely for as long as 17 days. The changes in C3 were dramatic; serum concentration rose from 8 to 70 mg/100 ml, and C3b could no longer be detected. A second metabolic study during this normalization period showed a decrease in fractional catabolic rate toward normal. The patient's histamine excretion was constantly elevated but increased further after a warm shower and after receiving normal plasma; at both times he had urticaria. These observations were consistent with the endogenous production of C3a and the resulting histamine release from mast cells. The inactivating mechanism for C3a was apparently intact in the patient's serum. The difference in the electrophoretic mobilities of C3b and C3c was shown as well as the electrophoretic heterogeneity of C3c. Suggestive evidence was also presented that the form of C3 with an activated combining site for red cells, previously postulated by others, is a transient C3 conversion product with an electrophoretic mobility slower than that of C3 on agarose electrophoresis.

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The pattern of lipid loss from the membrane of red cells incubated in serum is influenced by the availability of glucose. Under homeostatic conditions with respect to glucose, cholesterol alone is lost. This results from esterification of free cholesterol in serum by the serum enzyme, lecithin:cholesterol acyltransferase, and is associated with a proportional decrease in membrane surface area, reflected by an increased osmotic fragility. This selective loss of membrane cholesterol also occurs in hereditary spherocytosis (HS) red cells, even after incubation for 65 hr in the presence of glucose. The loss of free cholesterol from red cells relative to its loss from serum, under these conditions, is greatest at higher hematocrits, similar to those found in the spleen. Although the selective loss of membrane cholesterol increases the spherodicity of normal red cells, it does not lead to a change in their rate of glucose consumption, and both the loss of cholesterol and the increase in osmotic fragility are reversible in vitro. Moreover, normal red cells made osmotically fragile by cholesterol depletion in vitro rapidly become osmotically normal and survive normally after their reinfusion in vivo.In contrast to this selective loss of membrane cholesterol, red cells incubated in the absence of glucose lose both cholesterol and phospholipid. This occurs more rapidly in HS than normal red cells and is followed by a disruption of cation gradients and then by hemolysis. Cholesterol and phospholipid lost under these conditions is not restored during subsequent incubations in vitro. Selective loss of membrane cholesterol is a physiologic event secondary to an altered state of serum lipids. It is reversible both in vitro and in vivo and neither influences cellular metabolism nor impairs viability. Conjoint loss of phospholipid and cholesterol, however, results from intrinsic injury to the red cell membrane which results from prolonged metabolic depletion.

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The fate of small doses of isotopically labeled isologous hemoglobin was studied in the rat. When haptoglobin depleted animals were given 2.0 mg of (59)Fe hemoglobin intravenously, nearly half was trapped by the kidneys. Kidney (59)Fe activity disappeared slowly over several weeks. Whatever iron was lost from the kidneys was largely reutilized. In contrast, the porphyrin of hemoglobin absorbed by the kidneys appeared to be rapidly catabolized, since 5 hr after the injection of (14)C or (59)Fe heme-labeled hemoglobin only a small fraction was recovered as hematin. Likewise, after injection of globin-labeled hemoglobin, rapid disappearance of kidney protein activity indicated that the absorbed globin was readily catabolized in situ.

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Red cells in hereditary spherocytosis (HS) have a decreased ratio of membrane surface area to cell volume and therefore a spheroidal shape. This abnormality in shape predisposes them to pooling and destruction in the spleen. Although splenectomy prevents hemolysis in HS, the red cell defect, as manifested by spheroidicity, increased autohemolysis, excesive permeability to sodium, and hypermetabolism, persists. The role of membrane lipids in these manifestations in vitro and in cell survival in vivo was examined. Before splencetomy, and in spite of the presence of a young cell population, the cholesterol and phospholipid content of HS red cells is decreased. After splenectomy lipid values are similar to those obtained in normal subjects with spleens. However, after splenectomy for conditions other than HS the lipid content of red cells is greater than normal. Thus, when compared with the red cells of patients without HS who have also undergone splenectomy, HS cells after splenectomy are deficient in both cholesterol and phospholipid. Obstructive jaundice causes an increase in membrane lipid, primarily cholesterol, and a decrease in the osmotic fragility of normal red cells. When HS red cells are transfused into patients with obstructive jaundice they also become less osmotically fragile. Moreover, when incubated in obstructive jaundice serum, they gain cholesterol. This acquistion of membrane lipid in vitro does not result in a change in their rate of glucose utilization or sodium efflux. However, the transformation to a less spheroidal shape in vivo permits them to traverse better the splenic circulation and survive longer.

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