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Biomedical subjects

H de Groot

Publications and source records attributed to H de Groot.

At least 73 records · Page 4Linked to original sources
PubMed1996

Birch pollinosis and atopy caused by apple, peach, and hazelnut; comparison of three extraction procedures with two apple strains.

This study aimed, first, to study the prevalence in The Netherlands of atopy caused by apple, peach, and hazelnut in patients with tree pollinosis, and, second, to compare three extraction procedures for skin prick testing with two different apple strains. Skin prick tests and RAST were performed on 79 consecutive patients with tree pollinosis, visiting the department of allergology during spring 1995. In skin prick tests, we used three different extracts (juice, freeze-dried extract, and low-temperature acetone powder extract) of two apple strains, Golden Delicious and Granny Smith. Case histories for apple, peach, and hazelnut were positive in 35 (44.3%), 23 (29%), and 35 (44.3%) patients, respectively. More than two-thirds of the patients had symptoms characteristic of oral allergy syndrome. Skin prick tests for apple, peach, and hazelnut were positive in 51 (64.6%), 61 (77.2%), and 71 (89.9%) patients, respectively. Granny Smith showed more positive skin reactions and a better agreement with clinical history than Golden Delicious, and juice was superior to the two other extraction procedures for both apple strains. RAST for apple, peach, and hazelnut was positive in 53 (68.8%), 13 (16.9%), and 31 (40.3%) patients, respectively. Concordance between skin prick test and case history was found in 77%, 52%, and 54%, for apple, peach, and hazelnut, respectively. We found a high percentage of concurrence of clinical allergy to birch pollen and apple, peach, and hazelnut, confirmed by both skin prick testing and RAST. Approximately half of these patients had symptoms (especially oral allergy syndrome) after eating these products. We also found an easy extraction procedure (juice extract) suitable for apple skin prick testing, superior even to freeze-dried extraction or the low-temperature acetone powder technique.

Adolescent↗
PubMed1996

[Auxiliary liver transplantation in urgent and emergency indications].

This report will focus on seven patients treated with auxiliary liver transplantation. In two cases the indication was severe metabolic disorder and in five cases a fulminant hepatic failure. The clinical course was highly complicated in both cases with metabolic disorder (the transplant was lost, one patient died), but satisfactory in the patients suffering from fulminant hepatic disease: three of five are off immunosuppression, one is under therapy and one patient died of sepsis in the early phase.

Adolescent↗
PubMed1995

Allergy to bumblebee venom. I. Occupational anaphylaxis to bumblebee venom: diagnosis and treatment.

We describe six patients with severe occasional anaphylaxis, caused by stings of bumblebees. Sensitization to bumblebee venom was confirmed by intracutaneous tests and RAST with purified bumblebee venom. Three patients changed their occupation and will probably not be stung by bumblebees in the future. The other patients started immunotherapy with newly purified bumblebee venom extract. After 1 year of treatment, no severe side-effects had occurred and clinical benefit in two patients could be demonstrated, as both skin sensitivity or serum IgE to bumblebee venom had decreased. Moreover, both patients were unresponsive to in-hospital sting challenge.

Adult↗
PubMed1995

Drug-dependent exercise-induced anaphylaxis.

Exercise-induced anaphylaxis (EIA) is well known and may be food-dependent. We describe a patient with a history of anaphylaxis during exercise after taking nafylpropion acid (Naprosyne), a nonsteroidal anti-inflammatory drug. An exercise-challenge test after Naprosyne intake induced bronchoconstriction. The combination of history and challenge tests suggests that intolerance or allergy to drugs may present as EIA.

Adolescent↗
PubMed1994

Integrins and osteoclastic resorption in three bone organ cultures: differential sensitivity to synthetic Arg-Gly-Asp peptides during osteoclast formation.

We investigated possible inhibitory effects of five synthetic Arg-Gly-Asp (RGD)-containing peptides on osteoclastic resorption in three distinct in vitro resorption assays (17-day-old fetal mouse bone organ cultures) that differ in stages of osteoclast differentiation. RGD peptides, which can bind the adhesion receptors called integrins, inhibited osteoclastic resorption (45Ca release) in fetal mouse bone explants in which osteoclast precursors have yet to adhere to the mineralized matrix and develop into mature osteoclasts (metacarpals and coculture system). Treatment of metacarpals with RGD peptides inhibited the formation of multinucleated TRAP+ osteoclasts in the mineralized matrix because their mononuclear TRAP+ osteoclast precursors remained localized in the periosteum. In particular, echistatin, a viper venom protein with known affinity for alpha v beta 3 integrin, and GdRGDSP inhibited osteoclastic resorption dose dependently in these systems (ED50 10(-9) and 10(-4) M, respectively) but did not alter the activity of mature resorbing osteoclasts in radii. In addition, 45Ca release was significantly inhibited by the cyclic peptide GPenGRGDSPCA, which has a relatively higher affinity for the vitronectin than fibronectin receptor(s). In contrast, GRDGdSP, which has a much higher affinity for the fibronectin receptor (than the vitronectin receptors), had no effect on resorption at similar concentrations in any resorption system used. In summary, the data presented in this paper show that peptides with RGD motifs are capable of inhibiting osteoclastic resorption in bone organ cultures. Our studies not only support the hypothesis concerning the importance of alpha v beta 3 in osteoclastic resorption but also suggest an important role of integrin(s) in events preceding the actual resorption of calcified matrix by osteoclasts.

Amino Acid Sequence↗
PubMed1994

Nonparenchymal cell and hepatocellular injury to human liver grafts assessed by enzyme-release into the perfusate.

Experimental studies have demonstrated preferential injury to the sinusoidal endothelium during liver preservation with University of Wisconsin (UW) or Euro-Collins solution. This endothelial cell injury has an unclear pathogenesis, and it has not yet been studied in the human liver. Therefore, we analyzed the effluent of 21 human liver allografts after cold storage. Markers of hepatocellular and nonparenchymal cell injury were assessed. After preservation with UW solution, early effluent samples contained 1823 +/- 1494 U/l lactate dehydrogenase (LDH), 493 +/- 516 U/l alanine aminotransferase (ALT) and 132 +/- 97 U/l creatine kinase (CK; 92 +/- 92 U/l CK-BB). The effluent of livers preserved in histidine-tryptophan-ketoglutarate (HTK) solution contained 3681 +/- 2009 U/l LDH, 1139 +/- 599 U/l ALT and 282 +/- 120 U/l CK (165 +/- 91 U/l CK-BB). Comparison of effluent enzyme activities with liver tissue enzyme activities indicates that the release of the endothelial cell/nonparenchymal cell marker creatine kinase was higher, by a factor of 7-8, than the release of hepatocellular enzymes. Effluent thrombomodulin concentrations were 123 +/- 248 ng/ml (UW) and 604 +/- 299 ng/ml (HTK), and effluent glucose concentrations, 40.3 +/- 27.0 mM (726 +/- 486 mg/dl; UW) and 10.4 +/- 4.5 mM (187 +/- 81 mg/dl; HTK). We conclude that prominent endothelial cell injury also occurs in human liver grafts after preservation with UW solution or HTK solution. This endothelial cell injury is unlikely to be caused by hypoxia-induced energy deficiency, as it affects a cell type with a high glycolytic capacity in the presence of high glucose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Antioxidant effects of estradiol and 2-hydroxyestradiol on iron-induced lipid peroxidation of rat liver microsomes.

In the present study, the antioxidant effects of estradiol (E2) and 2-hydroxyestradiol (2-OHE2) on microsomal lipid peroxidation induced by Fe3+/ADP/NADPH and Fe2+/ascorbate are described. The extent of lipid peroxidation was measured by thiobarbituric acid reactive substances (TBARS) detection, low-level chemiluminescence, and oxygen consumption. 2-OHE2 had a potent antioxidant activity, which in all cases was higher than that of E2. In the Fe2+/ascorbate model, 2-OHE2 showed a similar pattern of inhibition, irrespective of the presence of NADPH or the functionality of microsomes. However, E2 produced only a slight inhibition when either denatured microsomes or native microsomes without NADPH were used, whereas its protective effect increased considerably when microsomal E2 metabolism was favored. During enzymic Fe3+/ADP/NADPH-induced lipid peroxidation, both E2 and 2-OHE2 were found to provide good protection. Results underline the importance of the chemical structure of these compounds and the role of estradiol metabolism in its antioxidant effects.

Animals↗
PubMed1994

MHC antigen presentation on the surface of hepatocytes: modulation during and after hypoxic stress.

Presentation and recognition of MHC antigen on the surface of cells is the basic process of initiating rejection and distinguishing "self and not self". This is considered to begin when a transplanted organ is reperfused with the blood of the recipient. In this study, the modulation of MHC I antigen presentation during preservation was investigated in a cell culture model using primary hepatocyte cultures of male Wistar rats. By incubation with different preservation solutions used in clinical transplantation, expression of the MHC antigen was observed during cold hypoxia. Primary hepatocyte cultures were isolated from male Wistar rats by a modified Seglen technique and seeded to glass slides, thus obtaining monolayer cultures. After 1 day of resting the cultures were incubated under different conditions using Krebs Henseleit solution (KH), Euro-Collins solution (EC), HTK solution of Bretschneider (HTK) and University of Wisconsin solution (UW) as incubation media. The conditions of incubation were warm normoxia (37 degrees C, pO2 100 mm Hg) and cold hypoxia (4 degrees C, pO2 < 0.1 mm Hg), which is the main condition of organ preservation. Incubation time was 6 h. Before starting the incubation reference cultures were fixed and every 60 min several cultures were withdrawn from the experiment and fixed also. MHC expression was studied by staining the cultures with monoclonal antibodies against rat MHC class I and class II. As expected, MHC class II was not present on the surface of hepatocytes, while MHC class I was demonstrated on the controls as well as on the cultures that were incubated using KH and EC independent of temperature and hypoxia or normoxia. At the end of the incubation they were still positive but not as strong as in the beginning. During incubation using HTK and UW, MHC I was not detectable at all phases of the experiment. In conclusion, hypoxic stress did not completely eradicate MHC I expression in rat hepatocytes, while the composition of the preservation medium may result in a hepatocyte surface negative for MHC I. Hydroxyethylstarch may be the substance in UW that covers the MHC antigen, while in HTK, mannitol or the histidine complex may play the same role. MHC negativity of the cells of a preserved transplant is another reason for the benefit of UW or HTK.

Animals↗
PubMed1994

Reactive oxygen species in tissue injury.

Reactive oxygen species (free radicals) are constantly formed in biological systems. They are removed by enzymatic and non-enzymatic defense systems such as superoxide dismutases, catalase, glutathione peroxidases, vitamin E, glutathione and vitamin C. Tissue injury such as lipid peroxidation results from an increased formation of reactive oxygen species, e.g. by the mitochondrial respiratory chain or by activated phagocytic cells, and/or a decreased antioxidant defense including a decreased repair capacity. In antioxidant therapy several specific and potent antioxidants are required.

Animals↗
PubMed1994

The potential role of reactive oxygen species in liver ischemia/reperfusion injury following liver surgery.

Reperfusion of a previously ischemic tissue may lead to an aggravation of injury. The liver has been shown to be susceptible to this reperfusion injury in several experimental systems. Reactive oxygen species appear to play an important role in the development of such injury, as has been demonstrated by direct measurements of their release, and by the protective effects of antioxidants. Upon reperfusion, reactive oxygen species may be released by hepatocytes, Kupffer cells and neutrophils. The relative contribution of the various liver cell types to the release of reactive oxygen species depends on several factors, including the duration and condition of ischemia and the time elapsed after reperfusion. There is only limited evidence for the occurrence of reperfusion injury in humans following liver surgery. The role of reactive oxygen species in this injury in humans remains to be shown.

Animals↗
PubMed1994

[Liver transplantation in halothane-induced liver necrosis].

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.

Adult↗
PubMed1994

[Differences in the mechanisms of damage to Kupffer cells and liver endothelial cells during preservation in UW solution].

AIM OF THE STUDY: The predominant injury during cold preservation of the liver appears to affect the non-parenchymal cells. Therefore we studied the contribution of hypoxia and the effect of the University of Wisconsin (UW) solution on the injury to cultured liver endothelial and Kupffer cells. METHODS: Cultured endothelial cells and Kupffer cells of the rat liver were incubated in Krebs-Henseleit buffer at 37 degrees C and in both, Krebs-Henseleit buffer and UW solution, at 4 degrees C. Hypoxic conditions were simulated by the addition of cyanide (1 mM), to some of the cultures glucose (10 mM) was added. Cell injury was assessed by the uptake of the vital dye trypan blue and by the release of cytosolic lactate dehydrogenase. RESULTS: Kupffer cells as well as endothelial cells exhibited a high hypoxia tolerance in Krebs-Henseleit buffer at both 37 degrees C and 4 degrees C. A large difference between both cell types, however, was seen during cold incubation in UW solution: whereas only 35 +/- 10% of Kupffer cells lost viability during 24 hrs under aerobic control conditions, the loss of viability of liver endothelial cells was already 83 +/- 12% under the same conditions. The addition of KCN increased the Kupffer cell injury to 75 +/- 8% but strongly decreased the endothelial cell injury to 3 +/- 2%. The addition of glucose to the cyanide-containing UW solution decreased the injury to Kupffer cells but increased the injury to endothelial cells. CONCLUSION: During cold incubation in UW solution cultured liver endothelial cells are affected by an energy-dependent injury. This type of injury is not detectable in Kupffer cells.

Adenosine↗
PubMed1994

[Changes in cytosol Ca(2+)-, Mg(2+)-, H(+)-, N(+)-, and K(+)-concentrations in cultivated hepatocytes in hypoxic conditions].

AIM: It is assumed that disturbances of cellular ion homeostasis, especially an increase in the cytosolic Ca2+ concentration, are of decisive importance for hypoxic cell injury. The aim of this study is the determination of alterations in the cytosolic Ca2+, Mg2+, H+, Na+ and K+ concentration in cultured hepatocytes during hypoxia. METHODS: The alterations of ion homeostasis under hypoxic conditions were studied in primary cultures of isolated rat hepatocytes by using fluorescence microscopy. RESULTS: The measurements of cytosolic Ca2+ concentration showed no alterations during the first 3-4 h of hypoxia. About 1-2 h before cell injury became evident Ca2+ increased from 147 +/- 28 to 385 +/- 31 nM. Similarly the cytosolic Mg2+ concentration increased from 0.63 +/- 0.05 to 1.42 +/- 0.11 mM in a late stage of hypoxia. In contrast, the cytosolic Na+ concentration increased continuously from 16 +/- 2 mM at start to 76 +/- 9 mM after 5 h of hypoxic conditions. The cytosolic K+ concentration remained constant for 2 h (129 +/- 7 mM) but then decreased down to 31 +/- 18 mM. The intracellular H+ concentration increased slightly under hypoxic conditions, the pH decreased from 7.35 +/- 0.02 to 7.19 +/- 0.04. CONCLUSION: The results indicate that cytosolic Ca2+ plays only a minor role in the pathomechanism of hypoxic hepatocellular injury but suggest an important role of the cytosolic Na+ concentration in this process.

Acid-Base Equilibrium↗
PubMed1994

Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and Wilson's disease.

The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n = 17; group B) and Wilson's disease (n = 12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.

Adult↗