PubMed Health⌕ Search

Biomedical subjects

J van Gool

Publications and source records attributed to J van Gool.

At least 19 recordsLinked to original sources
PubMed2001

Results of a questionnaire evaluating different aspects of personal and familial situation, and the methods of potty-training in two groups of children with a different outcome of bladder control.

OBJECTIVE: This study aimed to investigate the family situation, personal behaviour and current micturition habits, the time of beginning and the method of potty-training in two groups of children with different outcomes of bladder control. MATERIAL AND METHODS: Parents of 140 children, between 7 and 15 years old, filled in a questionnaire comprising 43 questions. They were divided into a symptom group (n = 73) and a symptom-free group (n = 67) according to the outcome of bladder control. RESULTS: Parents remembered clearly the method of training and the time of starting the potty-training to achieve continence in their child, and the exact age at which these objectives were achieved. There was some confusion regarding the term incontinence: the majority of the parents (70%) considered their child to be continent in spite of day-wetting several times a week. All children with urge syndrome who had undergone a urodynamic investigation (n = 50) had an objective functional bladder disorder. CONCLUSIONS: Methods of training differed between the groups with and without lasting problems. The symptom group started training at a later age, had more tendency to punish and were more demanding when micturition did not start readily. The findings from the questionnaire strengthen the hypothesis that urge syndrome can be due to poor methods of potty-training. Very few parents searched spontaneously for help, which should prompt practitioners and paediatricians to be more alert to this problem.

Child↗
PubMed1999

Nocturnal enuresis: a suggestion for a European treatment strategy.

The objective of this study was to review the published literature on aetiology and treatment of nocturnal enuresis, with the aim of providing a treatment strategy which is easy for the patient and their family to follow. Results from European studies conducted over the last 15 y were included in this review. It can be concluded from the results of these studies that enuresis is the cause and not the result of a psychiatric disorder. However, there is still considerable variation in success rates, from 28 to 90%. It is of vital importance that a caring approach from the doctor and a positive family and patient attitude are present for successful treatment. The first choice of treatment should be the one most acceptable to the family, e.g. alarm, desmopressin and combination treatment.

Age Factors↗
PubMed1990

Alpha 2-macroglobulin and fibrinogen modulate inflammatory edema in man.

Animal experiments suggest that the response of acute-phase proteins (APPs) modulates the inflammatory reaction following tissue injury. To study this in man we investigated the relation between a number of APPs, including fibrinogen and alpha 2-macroglobulin, and the inflammatory edema induced by a primary immunization against cholera, typhoid, and yellow fever. Vaccination induces a significant APP response; however, only alpha 2-macroglobulin and fibrinogen were of importance to the amount of edema, measured 24 h after vaccination. High plasma levels of alpha 2-macroglobulin strongly inhibit the amount of edema, whereas a high level of fibrinogen proved to be a stimulating factor. This holds both for the basal prevaccination levels and the postvaccination levels. The normal variation of the plasma concentration of these proteins in healthy subjects seems to be a determining factor to the amount of edema in this kind of injury.

Acute-Phase Proteins↗
PubMed1990

The relation among stress, adrenalin, interleukin 6 and acute phase proteins in the rat.

Stress reactions exist in many conditions in which plasma interleukin 6 (IL-6) is elevated. Examples are burns and sepsis. In these situations fever is often present. These stress situations are always accompanied with high levels of adrenalin and corticosteroids. These hormones, especially when given together, elicit a definite response of acute phase proteins in normal rats. In two stress models, (i) laparotomy and (ii) fever induced by administration of PGE2 in the lateral intracerebral ventricle, we observed a rise of adrenalin and corticosteron followed by an elevated level of plasma IL-6. Therefore, we studied the effect of adrenalin and corticosteron on the plasma level of IL-6. Adrenalin evokes high levels of IL-6, and this effect can be blocked by propranolol. When IL-6 release is blocked in this way, the response of alpha 2 macroglobulin and the cysteine protease inhibitor, both fast-reacting acute phase proteins in rat, is strongly depressed. Isoprenalin, an adreno beta 2 agonist, also causes very high levels of IL-6, indicating that the release of IL-6 can be mediated by an adreno beta 2 receptor whose presence has been demonstrated in monocytic cells. The results suggest a relation between stress situations and IL-6 and may be another factor besides the presence of endotoxins, virus, etc. explaining the high levels of IL-6 observed in many serious clinical situations.

Acute-Phase Proteins↗
PubMed1989

[The effect of acute-phase proteins on inflammation edema due to vaccination].

The authors describe the profiles of a series of acute phase plasma proteins induced by vaccination (VAC) for cholera, typhoid, yellow fever and combinations of these with DTP. Cholera and typhoid VAC as single vaccinations induce the strongest reaction, yellow fever the weakest. The reaction pattern depends also on the kind of vaccination: DTP, especially, raises haptoglobin levels. Great individual variability in reaction exists. The authors also investigated the relation between the levels of these acute phase proteins, including alpha 2-macroglobulin, and the amount of inflammatory oedema that developed at the vaccination site. It was found that the pre-vaccination levels of alpha 2-macroglobulin and haptoglobin were correlated negatively with the oedema developed 24 hrs later, while fibrinogen showed a positive relationship. The acute phase reaction of these proteins did not alter these correlations. The other acute phase proteins had no influence on the oedema in this model. It is concluded that the existing substantial individual differences in plasma levels of alpha 2-macroglobulin, fibrinogen and haptoglobin in part govern the degree of oedema developing after a vaccination; they are to be regarded as factors of the so called 'innate immunity'.

Acute-Phase Proteins↗
PubMed1989

Effects of monocytic products, recombinant interleukin-1, and recombinant interleukin-6 on glycosylation of alpha 1-acid glycoprotein: studies with primary human hepatocyte cultures and rats.

Changes in the carbohydrate moieties of acute-phase glycoproteins (APGPs) often accompany the increase in their secretion by the liver during inflammation. In this study, we investigated whether factors known to regulate APGP gene expression are also involved in the altered glycosylation. For this purpose, the glycosylation pattern of alpha 1-acid glycoprotein (AGP) as secreted by human hepatocytes, cultured in the presence and absence of dexamethasone and monokines, was studied by crossed affino- (concanavalin A) immunoelectrophoresis (CAIE). The monokines rIL-1 and rIL-6, in the presence of dexamethasone, both stimulated AGP secretion and caused a change in glycosylation towards an increased Con A reactivity, including the appearance of two strongly reactive forms (D and E) normally not present. Dexamethasone alone did not influence either process. When tested in vivo in rats, rIL-6 also induced an increased presence of Con A-reactive forms of AGP in serum. In conclusion, the changes in secretion and glycosylation of AGP as seen during inflammation seem to be mediated by the same factor(s).

Acute-Phase Proteins↗
PubMed1988

Relation between acute-phase proteins and enhanced bleomycin-induced pulmonary fibrosis in the rat.

Intratracheal application of Bleomycin (Bleo) in rats induces interstitial pneumonitis followed by progressive fibrosis. As the presence of high levels of acute-phase proteins (= reactants = APR), especially alpha 2-macroglobulin of the rat (alpha 2M), enhances liver fibrosis, we investigated whether this phenomenon also occurs in rats with Bleo-induced lung fibrosis. The experiments showed that this is the case; lung fibrosis assessed by measuring hydroxyproline, hexosamine, and prolyl-4-hydroxylase was enhanced when just before Bleo application an acute-phase reaction was induced. This effect can be explained by the inhibitory effect of alpha 2M on collagenase. The experiments showed a significant positive correlation between alpha 2M and parameters of fibrosis. This is especially the case in the third week after Bleo application. Bleo itself does not induce a strong acute-phase reaction, notwithstanding the pneumonitis during the first weeks. The increased fibrosis is accompanied by progressive ventilatory disturbances demonstrated by high arterial pCO2 and low pO2. In patients undergoing Bleo treatment, varying levels of APR can be expected, and this could explain the rapid development of fibrosis in individual cases.

Acute-Phase Proteins↗
PubMed1988

Rat alpha 2 macroglobulin is a selective inhibitor of antigen-induced leucotrienes in rat isolated lungs.

Exogenously administered, purified rat alpha 2 macroglobulin (alpha 2M, recognized as an acute phase reactant with anti-inflammatory properties) greatly inhibits the increase of the pulmonary resistance during the antigen-induced bronchoconstriction in rats in vivo, whereas a BaSO4 pretreatment (a method to induce a broad spectrum of serum acute phase reactants, including alpha 2M) covers a broader bronchoprotection: suppression of the decrease of the dynamic lung compliance as well. To explain these differences we studied the influence of both alpha 2M and BaSO4 on the antigen-induced bronchoconstriction in rat isolated lungs in relation to the mediator release in lung-effluents. We report here that in this model alpha 2M only inhibits the antigen-induced SRS-A release, whereas the concomitant release of histamine and 5-HT was unaffected. As distinct from alpha 2M the BaSO4 pretreatment suppressed both the antigen-induced bronchoconstriction and the histamine, 5-HT and SRS-A release to a high extent. These data suggest that alpha 2M can be considered as a selective inhibitor of leucotrienes, which offers an explanation for several anti-inflammatory properties of alpha 2M, including protection against the antigen-induced increase of the pulmonary resistance in vivo.

Airway Resistance↗
PubMed1988

Fever and acute phase reactants in the rat.

In rats synthesis of some acute phase reactants can be induced by a combination of corticosteroids and adrenaline. During fever both hormones show high plasma levels. We studied the effect of fever induced by intra-cerebroventricular (i.c.v.) injection of PGE2 on the acute phase response. Fever was continuously recorded and 24 h after induction acute phase reactant (APR) response was measured as indicated by the rise of alpha-macrofetoprotein (alpha M FP, alpha 2 macroglobulin of the rat). Controls received 0.9% saline i.c.v. Controls did not develop fever (dTmax less than or equal to 1 degree C) nor did they show significant APR response. The maximal rise in body temperature after PGE2 (2.6 +/- 0.7 degrees C) correlated significantly with the rise in alpha M FP concentration 24 h later. Adrenalectomy prevented the APR response completely but the magnitude of the fever reaction remained the same (2.1 +/- 0.3 degrees C). alpha-Blockade gave a smaller fever response but had no effect on the APR response. In alpha- and beta-blockade, fever response was normal but no APR response was obtained. Destroying the sympathetic nerve supply to the liver with 6-OH dopamine retarded the fever response but again APR response was not impeded. In order to differentiate between the role of fever as such and the effect of PGE2 on APR synthesis, we used heat exposure to induce hyperthermia in normal rats who showed an APR response comparable with that after i.c.v. PGE2. Pretreatment with sodium salicylate before inducing hyperthermia led to a variable rise in alpha M FP. Fever as such, without tissue injury, induces an APR response. The pathway to this effect probably involves circulating corticosterone and adrenaline, possibly via a beta-receptor mediated stimulation.

Acute-Phase Proteins↗
PubMed1987

Correlation between electroencephalographic and biochemical indices in acute hepatic encephalopathy in rats.

Changes in biochemical and electroencephalographic parameters were followed over time during the development of acute hepatic encephalopathy (HE) in two different experimental models. In the rat, (sub)acute liver failure was obtained either by ligation of the hepatic artery in previously portacaval-shunted animals or by intraperitoneal injection of a high dose of galactosamine (GALN). The EEG changes were characterized in both models by a significant increase in low-frequency activity of the EEG power density spectra: the so-called 'left shift'. This 'left shift' was significant in liver ischemia after 4-5 h and in GALN hepatitis after about 30 h. The changes in plasma biochemical indices also showed a great similarity in both models. The concentration of all measured plasma amino acids (except histidine and arginine in GALN hepatitis and arginine in liver ischemia), NH3 and ALAT were significantly increased during the development of (sub)acute HE. Correlation of the combined data of electroencephalographic and biochemical indices showed a significant (P less than 0.01) correlation between the 'left shift' and NH3, taurine, threonine, proline, alanine, methionine, cystathionine, phenylalanine, tryptophan, ornithine and histidine. It is concluded that EEG spectral analysis is a useful parameter for following the development of (sub)acute hepatic encephalopathy in relation to biochemical parameters.

Acute Disease↗
PubMed1987

The protective effect of a reduction in intestinal flora on mortality of acute haemorrhagic pancreatitis in the rat.

Both colectomy and intestinal lavage combined with kanamycin instillation proved effective in reducing mortality from sodium taurocholate-induced acute haemorrhagic pancreatitis (AHP) in the rat, supporting the concept that the intestinal flora must be considered a major factor influencing mortality in AHP in the rat. The results of this study are consistent with the clinical observation that abdominal sepsis is the most frequent cause of death in severe acute pancreatitis. The conclusions of the study advocate clinical trials in which besides established symptomatic treatment, intestinal decontamination is the main goal of therapy in severe acute pancreatitis.

Acute Disease↗
PubMed1986

Histophotometric estimation of volume density of collagen as an indication of fibrosis in rat liver.

The development of fibrosis in the liver of 16 rats treated for 1, 2, 3 or 4 weeks with CCl4, has been followed with chemical hydroxyproline determination and histophotometric analysis of histological sections stained with Sirius Red F3BA in saturated aqueous picric acid. The readings were taken with a scanning and integrating microphotometer and corrected for picric acid absorbance as a measure for mean protein mass per unit area of the section. It appears that the integrated absorbance readings of Sirius Red absorbing material in the section show a highly significant correlation with the hydroxyproline determinations. It is concluded that picrosirius photometry can be used to give a measure of the volume density of collagen in sections. An advantage of the photometric assay is that measurements are taken on the basis of the microscopic image, so that it is also possible to estimate collagen density in a selected area, e.g. a tumour formation amidst normal tissue, or to exclude necrotic areas.

Animals↗
PubMed1986

Mechanisms by which acute phase proteins enhance development of liver fibrosis: effects on collagenase and prolyl-4-hydroxylase activity in the rat liver.

Previous experiments showed that the presence of high levels of acute phase reactants (APR) enhance CCl4-induced liver fibrosis in the rat. A high correlation was found between the degree of fibrosis and alpha 2-macroglobulin of the rat (alpha 2-macrofetoprotein, alpha M-FP) used for monitoring the acute phase response. This acute phase reaction was provoked by epinephrine just before CCl4 treatment was started. In the present study we analyzed the effect of APR by repeating these experiments and estimating liver neutral collagenase with a synthetic substrate and endogenous collagen as a substrate, and liver prolyl-4-hydroxylase. A strong depression of liver collagenase activity was found in rats with a preceding acute phase reaction contrary to the rats that underwent CCl4 treatment only. A high level of alpha M-FP correlated negatively with collagenase activity. Also in vitro alpha M-FP proved to inhibit collagenase activity. Prolyl-4-hydroxylase was increased in the rats during acute phase reaction and correlated highly and positively with alpha M-FP, haptoglobin, and ceruloplasmin. Thus high levels of APR promote development of CCl4-induced fibrosis, partly by anticollagenase activity and partly because of enhancement of prolyl-4-hydroxylase activity. The latter phenomenon can also be explained by the presence of APR, but this has to be proved.

Acute-Phase Proteins↗
PubMed1986

Acute phase reactants enhance CCl4 induced liver cirrhosis in the rat.

High levels of acute phase proteins (acute phase reactants, APR) suppress acute inflammatory reactions in the rat. As many APR have antiprotease properties, including an anticollagenase activity, the effect of APR on the development of CCl4-induced liver fibrosis was investigated in rats. APR were provoked by repeated injections of epinephrine, inducing a broad spectrum of APR. This reaction can be monitored measuring alpha 2-macroglobulin levels in the rat (alpha 2-macrofetoprotein, alpha M FP). This protein was found to inhibit both acute galactosamine hepatitis and acute CCl4-induced liver toxicity. The animals with high levels of APR at the start of CCl4 treatment developed a more severe degree of fibrosis and cirrhosis than the control group in which no acute phase reaction was induced. Epinephrine alone had no such effects. Additionally, the APR positive group showed an initially lower degree of hepatocellular damage when compared to control animals. This uncoupling of liver cell damage and subsequent fibrosis may demonstrate that higher levels of APR might be important as to the development of cirrhosis, possibly based on the anticollagenase activity of these proteins.

Alanine Transaminase↗
PubMed1986

Experimental pancreatitis in the rat: role of bile reflux in sodium taurocholate-induced acute haemorrhagic pancreatitis.

Mortality of sodium taurocholate-induced acute haemorrhagic pancreatitis in the rat was prevented by biliary diversion. Bile reflux into the pancreas after the induction of pancreatitis is postulated to be a major factor affecting mortality of this popular model of acute pancreatitis. The reduction of pancreatic secretory volume during pancreatitis is thought to be the cause of this phenomenon. Bile reflux augments dehydration by its stimulation of ascites production. It is suggested that sodium taurocholate-induced pancreatitis in the rat can only be extrapolated to human disease if bile reflux indeed plays a significant role in acute pancreatitis in man.

Acute Disease↗
PubMed1986

Pathways of enzyme transfer in sodium taurocholate-induced acute hemorrhagic pancreatitis.

The pathways of enzyme transfer from the pancreas into the systemic circulation were analyzed in sodium taurocholate-induced acute hemorrhagic pancreatitis in the rat by estimating lipase concentrations in blood, lymph and ascites. During the first few hours of pancreatitis high enzyme levels were observed in thoracic duct lymph. However, cannulation of the thoracic duct did not prevent a significant increase in the lipase concentration in peripheral blood. The portal vein lipase concentration was found to exceed the peripheral values by approximately 10%. Extremely high concentrations of lipase were measured in the ascites collected during pancreatitis. When the ascites was transferred to the peritoneal space of healthy rats, a significant increase in the lipase concentration in peripheral blood was measured. This increase could not be prevented by transection of the parasternal lymphatics. It was concluded that the hematogenous rather than the lymphatic transport of lipase from the pancreas and the peritoneal surface is the most important pathway. In this respect, this study does not support thoracic duct drainage but advocates peritoneal lavage as a logical therapeutic measure to reduce the concentration of circulating toxic substances from the pancreas in acute pancreatitis.

Acute Disease↗
PubMed1986

Alpha 2 macroglobulin of the rat, an acute phase protein, mitigates the early course of endotoxin shock.

Normal rats and rats with high levels of alpha 2 macrofetoprotein (alpha M FP), an acute phase globulin induced by pretreatment with BaSO4 i.p., were injected with sublethal doses of endotoxin. One hour survival was better in the group with high levels of alpha M FP (36%) than in controls (9%). All rats receiving purified alpha M FP i.p. survived. Recovery of mean arterial blood pressure, expressed as the surface area under the curve, was significantly better in the groups with high alpha M FP levels. Leakage of i.v. administered human albumin was the same in control and BaSO4 pretreated rats. BaSO4 induces peritonitis which could explain the albumin leakage. Experiments were repeated therefore in rats pretreated with adrenaline which also initiates the production of alpha M FP. In this group, I h survival after endotoxin administration was 100% and albumin leakage was significantly less than in rats receiving either endotoxin only or BaSO4-pretreatment. In early endotoxin shock prostaglandins, including PGE2 a potent vasodilatator, are released into the circulation. From previous data it is known that alpha M FP prevents the vasodilatation and increased vascular permeability caused by PGE2. Rats with high levels of alpha M FP had a smaller fall in diastolic blood pressure after PGE2 administration than did controls with normal alpha M FP levels. The effects of alpha M FP on the haemodynamic events in early endotoxin shock could well be due to inhibition of PGE2 activity.

Animals↗