Internet as a source of medicines information (MI) among frequent internet users.

BACKGROUND: The internet is widely and increasingly used to search for health information. Previous studies have focused mainly on health information on the internet and not specifically on medicines information (MI). OBJECTIVES: The aim of this study was to explore the internet as a source of MI compared to other sources of MI; to identify those who use the internet as a source of MI; and to describe patterns of use of the internet as a source of MI. METHODS: A cross-sectional design employed a web-based questionnaire posted by patients' and other organizations as well as pharmacies on their websites during six weeks in the beginning of 2014. Logistic regression analysis was used to assess associations of background variables to the use of different MI sources. RESULTS: The most frequently used MI sources among respondents (n = 2489) were package leaflets (90%), pharmacists (83%), physicians (72%), and the internet (68%). According to a multivariate analysis, internet use for MI was associated with female gender, age <65 years, higher education, daily use of the internet, and continuous use of vitamins or herbals. MI was most commonly searched from a Finnish health portal (56%) and websites of pharmacies (41%). Of the respondents, nearly half (43%) used search engines to find information from the internet. The names of the medicinal product, symptom or disease were the most commonly used search terms. CONCLUSIONS: Well-educated, young women tend to search MI on the internet. Health care professionals should discuss reliable MI websites and tools that can help patients evaluate the reliability of information.

Incorporation of [3H]glucosamine into glycosaminoglycans in different cell culture conditions by rabbit aortic smooth muscle cells.

This study sought to elucidate the optimal cell culture conditions for studies concerned with the incorporation of [3H]glucosamine into glycosaminoglycans by rabbit aortic smooth muscle cells. The incorporation of radioactivity into extracellular sulphated glycosaminoglycans was linear for at least 72 h and that into pericellular sulphated glycosaminoglycans for up to 24 h. The incorporation of radiolabel into hyaluronic acid was linear only up to 12 h. In the exponential growth phase the incorporation of [3H]glucosamine into sulphated glycosaminoglycans and hyaluronic acid proved to be less marked than in the stationary growth phase, but the highest values were nevertheless obtained immediately after trypsinisation. When studied in the stationary growth phase, cell density and incorporation of [3H]glucosamine were positively correlated in the case of hyaluronic acid, but in the case of sulphated glycosaminoglycans there was a negative correlation. The serum concentration of the incubation medium and the incorporation of radioactivity into hyaluronic acid were positively related. With sulphated glycosaminoglycans this was the case only after a 7-day preincubation in the different serum concentrations. When incorporation was studied without preincubation, the incorporation of radioactivity into sulphated glycosaminoglycans proved to be negatively associated with the serum concentration of the medium. The environmental pH of the cells was associated with the incorporation of radioactivity into hyaluronic acid and sulphated glycosaminoglycans in that between pH values 6.8 and 7.9 the incorporation of radioactivity increased when the pH of the medium was raised.

The triglyceride issue revisited. Findings from the Helsinki Heart Study.

BACKGROUND: In clinical practice, high triglyceride level is recognized as an indicator of increased risk of coronary heart disease (CHD), while most epidemiological studies have shown that triglyceride level is not an independent risk factor for CHD. In an effort to explain this discrepancy we reanalyzed the Helsinki Heart Study data in the light of findings from recent clinical studies related to the insulin resistance syndrome. METHODS: The log-linear modeling technique was used to study the pattern of cross-sectional interdependence of triglyceride level, high-density lipoprotein cholesterol (HDL-C) level, low-density lipoprotein cholesterol level, blood pressure, and blood glucose level. The CHD risk associated with different combinations of levels of triglycerides, HDL-C, and blood pressure was assessed via Cox proportional hazards models. RESULTS: Triglycerides occupied a central role in the pattern of associations of the factors studied; in particular, the associations with HDL-C level, blood pressure, and blood glucose level were without threshold values. The prevalence of high triglyceride level plus low HDL-C level was strongly associated with blood pressure and blood glucose level, while the prevalence of low HDL-C level alone was not. Only the subgroup with both high triglyceride and low HDL-C levels showed a substantial CHD risk, while those with low HDL-C levels alone or high triglyceride levels alone showed a marginal risk. CONCLUSIONS: Our results suggest that triglycerides play a central mediating role in the occurrence of several CHD risk factors, especially those related to the insulin resistance syndrome. Because of these interdependencies, the question of an independent effect of triglycerides is not relevant, and when assessing CHD risk, triglycerides should be considered jointly with HDL-C.

Long-term effect of hyperlipidemic serum on the synthesis of glycosaminoglycans and on the rate of growth of rabbit aortic smooth muscle cells in culture.

Rabbit aortic smooth muscle cells (SMCs) were successfully subcultured in 10% hyperlipidemic rabbit serum (HLS) for at least 9 passages. SMCs grown in HLS grew into higher cell densities than SMCs cultured in normolipidemic rabbit serum (NLS) for at least 4-5 passages in NLS and HLS, respectively. However, cells cultured in NLS and HLS for up to 7 passages had similar growth characteristics when they were trypsinised and seeded to grow in 10% fetal calf serum (FCS). Incorporation of [3H]glucosamine into GAGs was taken to represent their rate of synthesis. As compared with cultures incubated in 10% NLS, incubation of rabbit aortic SMCs in the presence of 10% HLS increased the synthesis of sulphated GAGs secreted into the pericellular space by 35% during the first 24 h of contact with HLS. After preincubation for one week in the presence of HLS the synthesis of sulphated GAGs secreted into the incubation medium and into the pericellular space was stimulated by 95% and 34%, respectively. The stimulation of the synthesis of sulphated GAGs by HLS continued for up to 4 weeks at least if the contact of the cells with HLS was maintained. When the cells were subcultured in the presence of NLS and HLS and seeded to grow in FCS after the 1st, 3rd and 7th trypsinisations, the synthesis of sulphated GAGs in cultures of cells from both sources was similar.

Effect of hypoxia on the synthesis of glycosaminoglycans and collagen by rabbit aortic smooth muscle cells in culture.

This study evaluated the effect of hypoxia on the connective tissue metabolism of rabbit aortic smooth muscle cells (SMCs) in culture. When the oxygen saturation of the incubation medium was lowered from 20% to 2-3%, synthesis of sulphated glycosaminoglycans (GAGs) and hyaluronic acid, as determined from the incorporation of [3H]glucosamine, was stimulated. However, this occurred only after 24 h preincubation of the SMCs in hypoxia. The collagen synthesis of the cells was determined from the incorporation of [3H]proline into protein hydroxyproline and calculated in mass units from the specific intracellular precursor radioactivity. The total protein synthesis was similarly determined from the incorporation of [3H]proline into protein-bound proline. Hypoxia decreased the collagen synthesis, but did not affect the total protein synthesis of the cells. When compared with the control cultures the cell protein of the SMC cultures kept in hypoxia, decreased on the first day in hypoxia whereafter it increased. These results may explain the mechanisms by which hypoxia affects the connective tissue metabolism of the arterial wall in vivo.

Enhanced growth of smooth muscle cells from atherosclerotic rabbit aortas in culture.

It has been suggested that cells in atherosclerotic lesions differ from normal arterial smooth muscle cells. The present study was aimed at elucidating this possibility. The morphology and growth characteristics of cells cultured from atherosclerotic rabbit aortas were compared with those obtained from control rabbits of the same age. Primary cultures were started from aortic intima-medial explants and they were subcultured after trypsinising the outgrowths. There were no differences in morphology between cells cultured from atherosclerotic and control animals as judged with phase contrast and electron microscopy. However, both the primary and subsequent growth rates of the cells cultured from atherosclerotic aortas were higher than those of control cells. Also the uptake of [3H]thymidine by cells derived from the atherosclerotic aortas was enhanced both in the exponential and stationary phases of cell growth. The results suggest that although the cells from atherosclerotic aortas are morphologically similar to normal arterial smooth muscle cells, atherogenesis is associated with the development of metabolic changes in the arterial cells that are carried over to daughter cells and persist even in culture.

Enhanced synthesis of collagen and total protein by smooth muscle cells from atherosclerotic rabbit aortas in culture.

Protein synthesis in smooth muscle cells from normal and atherosclerotic rabbit aortas was studied. Cultures of cells from the third passage were incubated with [3H]proline and the synthesis rates of collagen and total protein measured from the radioactivities incorporated into protein-bound hydroxyproline and proline, respectively. The synthesis ratio of collagen types I and III was studied by separating the radioactive procollagens of the culture media by DEAE column chromatography. The synthesis rates of both collagen and total protein were higher in cells cultured from atherosclerotic rabbit aortas. There was no difference in the synthesis ratios of types I and III collagen between cells from the two origins. In addition to procollagens, a third protein eluted before procollagen I in the DEAE chromatography of medium proteins. Compared with control cells, cells from atherosclerotic aortas incorporated relatively less radioactivity into this protein. No differences were detected in the amino acid compositions of cellular proteins between cells from both origins. It was concluded that cells grown from atherosclerotic rabbit aortas synthesize more collagen and total protein than those from normal aortas, the synthesis of collagens I and III being equally enhanced. The results also suggest that there are proteins which are not involved in the general enhancement of protein synthesis.

Metabolism of glycosaminoglycans and lipids in smooth muscle cells from atherosclerotic rabbit aortas in culture.

Glycosaminoglycan (GAG) and lipid synthesis in smooth muscle cells cultured from normal and atherosclerotic rabbit aortas were studied. The incorporation of [14C]glucosamine into acidic GAGs taken to represent their synthesis rate, was enhanced in cells from atherosclerotic aortas as compared with controls. The synthesis of sulphated glycosaminoglycans was affected most and the percentage of radioactivity incorporated into sulphated GAGs was 48 +/- 3% in cells from atherosclerotic and 38 +/- 4% in cells from healthy aortas. Non-radioactive GAGs secreted into incubation media were fractionated by electrophoresis. There was an elevated ratio of sulphated GAGs to hyaluronic acid in the cultures of cells from atherosclerotic aortas and the fraction corresponding to dermatan sulphate was increased most. The incorporation of [3H]oleate into phospholipids was enhanced in cells from atherosclerotic aortas indicating more rapid synthesis of this lipid fraction in these cells. Concentrations of free and esterified cell cholesterol were similar. The results indicate that the enhanced synthesis of sulphated GAGs typical of proliferative atherosclerosis in vivo is maintained in the third passage cultures of cells from atherosclerotic rabbit aortas. In addition there was an enhancement in the synthesis of phospholipids in these cells.

Comparison of peak serum C-reactive protein and hydroxybutyrate dehydrogenase levels in patients with acute myocardial infarction treated with alteplase and streptokinase.

Peak serum C-reactive protein concentrations were measured in 146 patients randomized to receive streptokinase, alteplase, or a combination of streptokinase and alteplase in the GUSTO-I trial. Those receiving alteplase treatment had lower values than those receiving streptokinase or the combination treatment. Irrespective of treatment, complete reperfusion of the infarct-related artery (TIMI grade 3 flow) was associated with low peak serum C-reactive protein values.

Ergosterol content in various fungal species and biocontaminated building materials

This paper reports the ergosterol content for microbial cultures of six filamentous fungi, three yeast species, and one actinomycete and the ergosterol levels in 40 samples of building materials (wood chip, gypsum board, and glass wool) contaminated by microorganisms. The samples were hydrolyzed in alkaline methanol, and sterols were silylated and analyzed by gas chromatography-mass spectrometry. The average ergosterol content varied widely among the fungal species over the range of 2.6 to 42 &mgr;g/ml of dry mass or 0.00011 to 17 pg/spore or cell. Ergosterol could not be detected in the actinomycete culture. The results for both the fungal cultures and building material samples supported the idea that the ergosterol content reflects the concentration of filamentous fungi but it underestimates the occurrence of yeast cells. The ergosterol content in building material samples ranged from 0.017 to 68 &mgr;g/g of dry mass of material. A good agreement between the ergosterol concentration and viable fungal concentrations was detected in the wood chip (r > 0.66, P 0.48, P 0.63, P < 0.0001). In conclusion, the ergosterol concentration could be a suitable marker for estimation of fungal concentrations in contaminated building materials with certain reservations, including the underestimation of yeast concentrations.

Effects of chronic oral nicotine treatment and its withdrawal on locomotor activity and brain monoamines in mice.

The effects of chronic nicotine and its withdrawal on locomotor activity and brain monoamines were studied using a new animal model of administering nicotine in the drinking water to male NMRI mice as the sole source of fluid. Locomotor activity as well as cerebral concentrations of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), noradrenaline (NA) and 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG) were measured post mortem on the 50th day of nicotine administration or at 12-14 or 23-25 h after withdrawal. On the 50th day of drug administration the chronically nicotine-treated mice were more active than the control mice drinking tap water and after withdrawal from nicotine the locomotor activity dropped to the level of the controls. In chronically nicotine-treated mice the striatal concentrations of DOPAC, HVA and 5-HIAA, hypothalamic 5-HIAA and NA as well as cortical NA were elevated. The concentrations of DOPAC, HVA and 5-HIAA reversed to control levels within 23-25 h after withdrawal from nicotine. The nicotine-induced elevation of the hypothalamic NA concentration was still significant at 23-25 h after withdrawal. At 12-14 h after withdrawal the hypothalamic concentration of MOPEG was increased. In conclusion, our findings on locomotor activity suggest that administration of nicotine in the drinking water to mice for several weeks seems to be a relevant method to study nicotine dependence. Furthermore, the alterations found in cerebral DA, NA and 5-HT metabolism during chronic nicotine administration indicate that all three cerebral transmitter monoamines might be involved in nicotine dependence and withdrawal.

Tolerance to nicotine's effects on striatal dopamine metabolism in nicotine-withdrawn mice.

After 7-week chronic administration of nicotine to mice in their drinking water, nicotine was withdrawn for 24 h. Acute nicotine challenge (1 mg/kg s.c., 60 min) elevated the striatal concentrations of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) and decreased the concentration of 3-methoxytyramine significantly less in the mice withdrawn for 24 h from nicotine than in the control mice which had been drinking tap water under identical conditions for 7 weeks. Neither withdrawal nor the acute nicotine challenge altered the striatal dopamine concentration. No alterations were found in the density or affinity of the specific binding of [3H]SCH 23390 or [3H]spiperone to striatal membrane homogenates during nicotine treatment or after its withdrawal. Thus, our results show that tolerance to the acute effects of nicotine on striatal dopamine metabolism can be induced by administering nicotine to mice in the drinking water. However, neither chronic nicotine treatment nor its withdrawal seem to affect dopamine D1 and D2 receptors in the striatum.

Chronic oral nicotine administration affects the circadian rhythm of dopamine and 5-hydroxytryptamine metabolism in the striata of mice.

The effect of chronic oral administration of nicotine on the circadian rhythm of striatal dopamine (DA) and 5-hydroxytryptamine (5-HT) was studied in mice. Mice receiving nicotine in their drinking water and control mice drinking tap water were killed at 05:00, 11:00, 15:00 or 21:00 hours on the 50th day of chronic administration. The plasma concentrations of nicotine and cotinine, as well the striatal concentrations of DA, 5-HT and their metabolites 3,4 dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT), homovanilic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were estimated. The largest plasma concentrations of nicotine and cotinine were found at 05:00, when they were more than double the concentrations found at the other times studied. This indicates that the mice, typically for nocturnal animals, consumed most of their daily drinking water at night. In the control mice, the striatal DA and 3-MT concentrations showed circadian variation and were lowest at 11:00. The 5-HIAA concentrations also varied, being highest at 11:00. In the nicotine-treated mice the circadian variations in striatal monoamines were altered and more pronounced than in the controls. The concentrations of DA, DOPAC, HVA and 5-HIAA were highest at 11:00 and that of 5-HT at 21:00. The striatal DA, DOPAC, HVA and 5-HIAA concentrations in the nicotine-treated mice were significantly higher at 11:00 and the 5-HT concentrations at 21:00 than in the control mice, and, in contrast to the control mice, in the mice treated with chronic nicotine no circadian rhythm was observed in the 3-MT. No elevation of striatal DA metabolites occurred in the nicotine-treated mice compared with the controls when the plasma nicotine concentration was at its peak at 05:00. This finding suggests development of tolerance to the nicotine-induced changes in striatal DA metabolism. Further, our findings suggest that the chronic administration of nicotine in the drinking water of mice alters the circadian pattern of striatal DA and, to a lesser extent, that of 5-HT, and thus may affect the functions regulated by these transmitters.

Regulation of nicotinic receptors in the brain of mice withdrawn from chronic oral nicotine treatment.

The effect of nicotine withdrawal on regional regulation of brain nicotinic receptors was studied in mice after chronic administration of nicotine in the drinking water for 2, 4 or 7 weeks. Two weeks of chronic nicotine administration did not alter the binding of [3H]-nicotine in the midbrain, cortex or cerebellum of the mice, while after both 4-and 7-week treatments a significant increase in the specific [3H]-nicotine binding was observed in cortical and midbrain membranes. In the midbrain, the [3H]-nicotine binding was increased by about 40% in mice withdrawn for 48-72 h from the 4-week chronic nicotine treatment and in mice withdrawn for 48 h from the 7-week treatment. The [3H]-nicotine binding was significantly increased (by 55-65%) in the cortex at 48 h and 72 h after withdrawal from 4-week chronic nicotine and it was even somewhat more increased (by 72-66%) after 7-week treatment. The cortical [3H]-nicotine binding was not altered at 24 h after the 4-week treatment, but in mice withdrawn for 24 h from the 7-week treatment it was increased by 116%. The increases in [3H]-nicotine binding returned to control levels within 1 week after withdrawal. None of the studied treatments affected the [3H]-nicotine binding in the cerebellum. Tolerance towards nicotine-induced locomotor depression was only found in mice withdrawn for 24 h from the 7-week chronic nicotine administration. These findings suggest that at least 4-week chronic nicotine administration in the drinking water is needed before any upregulation of nicotinic receptors can be observed. Furthermore, in our experiments the increase in the [3H]-nicotine binding was seen before behavioural tolerance could be demonstrated. The differences between brain regions in the time course of nicotinic receptor upregulation may reflect variations in nicotinic receptor subunits and their sensitivity to chronic nicotine treatment.

Chronic nicotine administration in the drinking water affects the striatal dopamine in mice.

Although tobacco contains a large variety of substances, its addictive properties are most probably due to the reinforcing actions of nicotine that motivates continued tobacco use. Animals and humans self-administer nicotine, a response that appears to involve the mesolimbic dopamine system and to be common to other abused drugs. The present article reviews animal models to administer nicotine chronically. We also describe a new animal model in which nicotine is given to mice in drinking water as their sole source of fluid. This treatment produced nicotine plasma concentrations comparable to or above those found in smokers. We found that mice withdrawn from nicotine were tolerant to the effects of nicotine challenge on striatal dopamine metabolism as well as on body temperature and locomotor activity. Furthermore, 3H-nicotine binding in the cortex and midbrain was significantly increased in mice withdrawn from nicotine. The last part of the article will focus on the effects of this chronic nicotine treatment on striatal dopamine. Dopamine and its metabolites and locomotor activity were increased in the forenoon in mice still drinking nicotine solutions. We also report recent data in which chronic nicotine administration in the drinking water enhanced the effect of dopamine receptor agonist, quinpirole, on striatal metabolism. The animal model described appears to be a relevant method for studying the mechanisms that are thought to be involved in nicotine dependence.

Enhanced motor activity and brain dopamine turnover in mice during long-term nicotine administration in the drinking water.

Nicotine was administered chronically to NMRI mice in their drinking water in gradually increasing concentrations to measure gross motor activity and brain nicotine concentrations over 24 h on the 50th day of nicotine administration. Also, the striatal postmortem tissue concentrations and accumbal extracellular concentrations of dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured to study the role of dopaminergic systems in nicotine-induced hyperactivity in mice. The cerebral nicotine concentration was at its highest at the end of the dark period. The activity of nicotine-treated mice and their striatal DA metabolism were parallelly increased at 2 to 3 h after midnight and in the forenoon. Microdialysis experiments carried out in the forenoon showed that the extracellular levels of DA and DOPAC were elevated in the nucleus accumbens of these mice. Nicotine did not alter the circadian rhythmicity of activity in the mice. Rather, our findings suggest that the mice consume more nicotine when active and this might lead to enhanced release and metabolism of DA and further, to enhanced motor behavior. These findings support the suggestions that nicotine's effects on limbic and striatal DA are critical for its stimulating effects.

Acute effect of dialysate calcium concentration and intravenous vitamin D3 on the secretion of parathyroid hormone in hemodialysis patients.

We studied the suppression of intact parathyroid hormone (PTH) in ten patients on chronic hemodialysis using different calcium concentrations of dialysate. Secondly, giving i.v. vitamin D3 at commencement of dialysis we investigated whether 1 alpha (OH)D3 or 1,25(OH)2D3 acutely modifies the responsiveness of the parathyroid gland to the suppressive effect of increased serum calcium. Dialysis with high-calcium dialysate (1.75 mmol/l) reverted the plasma PTH to normal limits. Lower-calcium dialysate (1.5 mmol/l) induced only a partial suppression of hyperparathyroidism. We found no differences in the suppression of hyperparathyroidism whether 1 alpha (OH)D3 or 1,25(OH)2D3 was given at the beginning of the dialysis or not. We conclude that the suppressibility of hyperparathyroidism in dialysis patients can be evaluated by different calcium concentrations of dialysate, and that i.v. vitamin D3 does not acutely modify the responsiveness of the parathyroid gland to the effect of calcium.

Measurement of serum ionized versus total levels of magnesium and calcium in hemodialysis patients.

Until recently, only techniques for measuring total magnesium have been available. Now commercially available instruments using new ion-selective electrodes (ISE) for Mg+2 have made possible reliable measurement of ionized magnesium also in clinical practice. We measured changes induced by a hemodialysis session in serum ionized and total pools of magnesium and calcium using ISE methods. When compared with levels in age- and sex-matched control subjects, both serum ionized magnesium (0.68 +/- 0.11 vs. 0.56 +/- 0.06 mmol/l, p < 0.001) and total magnesium (1.00 +/- 0.19 vs. 0.82 +/- 0.08 mmol/l, p < 0.001) were higher in hemodialysis patients. The fraction of ionized Mg was 68.6 +/- 2.9% in hemodialysis patients, and did not differ significantly from that in controls (68.7 +/- 5.3%). The postdialysis value was 68.1 +/- 7.7%. The corresponding ratios of calcium (ionized/total) were 51.0 +/- 2.8% pre- and 50.9 +/- 4.6% postdialysis. Both prior to and after dialysis the correlation between ionized and total magnesium was high (r = 0.976, p < 0.001, and r = 0.925, p < 0.001, respectively). The corresponding ionized versus total calcium correlations were r = 0.724 (p < 0.001) before and 0.423 (p = 0.003) after dialysis. The changes induced by a hemodialysis session in serum concentration of ionized magnesium and calcium were dependent on the concentration of the cation in the dialysate. The change in PTH (suppression or stimulation) was very closely related to the changes in the serum concentration of ionized calcium. We concluded that measurement of ionized magnesium using ion-selective electrodes for Mg++ is an interesting new method in evaluating body magnesium status. Its definitive role in clinical practice cannot be judged on the basis of the results of the present study, but it will probably not achieve the same importance as the measurement of ionized calcium in clinical nephrology.

Renal biopsy findings and clinicopathologic correlations in nephropathia epidemica.

A series of 126 adult patients with a serologically confirmed diagnosis of nephropathia epidemica (NE) were studied during the acute phase of the disease. In 86 cases, renal biopsy was performed. The severity of renal failure correlated slightly with blood inflammatory parameters and the degree of hematuria but not with the amount of proteinuria. The degree of hematuria correlated inversely with the level of thrombocytopenia. The most common histopathologic lesion was acute tubulointerstitial nephritis. Interstitial edema and inflammatory cell infiltrations were most usually present, followed by tubular epithelial and luminal alterations. Slight glomerular mesangial changes were present in 25% of the biopsy specimens. Except for hemorrhage in the outer renal medulla, the histologic lesions were relatively mild and unspecific. Interstitial hemorrhage should remind a pathologist of the possibility of NE. Tubular, interstitial and glomerular histologic damage were but vascular lesions were not associated with the clinical severity of renal failure. Glomerular alterations did not relate to the amount of urine protein excretion. Correlations, however, were so weak that in clinical work renal biopsy is usually not indicated for determination of the severity of renal failure in NE. Intrinsic renal events are probably important in the development of renal failure in NE.

Video disc recording in double contrast barium enema--comparison with conventional fluoroscopy.

The use of electronic radiography in double contrast enema reduced the fluoroscopic area exposure of three different radiologists by 48-63% compared with conventional fluoroscopy. The fluoroscopic technique in video disc recording (VDR) differs from the conventional fluoroscopic technique and therefore the use of VDR requires additional training.