Biomedical subjects

T Henriksen

Publications and source records attributed to T Henriksen.

At least 19 recordsLinked to original sources

PubMed2001

Analysis of acidic pesticides using in situ derivatization with alkylchloroformate and solid-phase microextraction (SPME) for GC-MS.

A solid-phase microextraction (SPME) method was developed for the analysis of acidic pesticide residues in water. The method utilizes in situ derivatization with butylchloroformate (BuCF), followed by on-line SPME extraction using a PDMS fibre, and analysis by GC-MS. Derivatives of the phenoxy acids mechlorprop (MCPP), dichlorprop (DCPP), MCPA and 2,4-D and their phenol degradation products 4-chloro-2-methylphenol and 2,4-dichlorophenol (DCP) were identified. Detection limits at 0.16-2.3 microg/l were achieved. Optimization of derivatization, ion strength, extraction time, SPME-fibre, desorption time and temperature are described. Standard curves in the range 0.5-10.0 microg/l were fitted to a second-degree polynomial. Standard deviation (n = 5) was below 10% for the phenol derivatives, but 20-50% for the phenoxy acids. For method verification groundwater samples from a field experiment were screened for content of MCPP and compared to the results from the HPLC analysis. A good agreement was obtained with respect to identification of positive samples, even though concentrations measured by the SPME were lower than with HPLC. Even if the precision and accuracy do not meet the demands for a strictly quantitative analysis, the SPME method is suitable for screening, because it is cheap, it can be automated, and uses smaller amounts of potential harmful solvents. Also, the method is less labour-intensive, as it requires a minimum of sample preparation when compared to traditional analyses. The acidic pesticides bentazon, dicamba, bromoxynil, ioxynil, dinoseb and DNOC were included in the study but could not be analysed by the current method.

Acids↗

PubMed2001

VEGF mRNA is unaltered in decidual and placental tissues in preeclampsia at delivery.

BACKGROUND: VEGF (vascular endothelial growth factor) is a growth factor which is central in blood vessel formation. We wanted to determine whether the mRNA levels of VEGF are altered in preeclampsia in decidual and placental tissues compared to control pregnancies. METHODS: Decidua basalis was obtained by vacuum aspiration during cesarean section in 25 preeclamptic and 19 uneventful pregnancies. Placental biopsies were taken immediately after delivery. Relative mRNA levels of VEGF were quantified and compared to those of the housekeeping gene beta-actin. RESULTS: No statistically significant differences in VEGF mRNA levels were found between the preeclampsia and the control group for either the decidual or placental tissues. Furthermore, there were no significant differences between VEGF mRNA levels in the preeclamptic and control group with respect to gestational age of the women. CONCLUSIONS: This study provides no evidence of abnormal VEGF expression at delivery in decidua basalis or placenta in pregnancies complicated by preeclampsia.

Adult↗

PubMed2001

High intake of energy, sucrose, and polyunsaturated fatty acids is associated with increased risk of preeclampsia.

OBJECTIVE: Preeclampsia is associated with high body mass index, insulin resistance, and hypertriglyceridemia. Our objective was to investigate prospectively whether diet in the first half of pregnancy is associated with the risk for preeclampsia. STUDY DESIGN: This prospective, population-based, cohort study of pregnant women investigated dietary intake early in the second trimester with a quantitative food frequency questionnaire. RESULTS: The questionnaire was completed by 3133 women (83%). Preeclampsia developed in 85 women. Adjusted odds ratio (95% CI) for preeclampsia was 3.7 (1.5-8.9) for energy intake of >3350 kcal/d compared with < or =2000 kcal/d. Adjusted odds ratio (95% CI) for preeclampsia was 3.6 (1.3-9.8) for sucrose intake (percent of total energy) of >25% compared with < or =8.5% and 2.6 (1.3-5.4) for polyunsaturated fatty acids intake (percent of total energy) of >7.5% compared with < or =5.2%. Other energy-providing nutrients were not associated with the risk for preeclampsia. CONCLUSION: The current study suggests that high intakes of energy, sucrose, and polyunsaturated fatty acids independently increase the risk for preeclampsia.

Adult↗

PubMed2001

8-iso-prostaglandin F(2alpha) increases expression of LOX-1 in JAR cells.

Lectinlike oxidized LDL receptor-1 (LOX-1), a cell-surface receptor for oxidized LDL (ox-LDL), is proposed to be involved in endothelial dysfunction and in the pathogenesis of atherosclerosis. Preeclampsia is a pregnancy complication diagnosed by hypertension and proteinuria, characterized by endothelial dysfunction, and supposedly caused by compounds from hypoxic uteroplacental tissues. A feature of preeclampsia is formation of foam cells in maternal arterial walls of gestational tissue ("acute atherosis"). Oxidative stress is believed to play a role in the pathophysiology of preeclampsia. 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) is a marker of oxidative stress in vivo, is biologically active in vitro, and is elevated in preeclamptic plasma and gestational tissue. In the present article, we hypothesized that 8-iso-PGF(2alpha) could induce the expression of LOX-1 in trophoblastic cells (JAR). We demonstrated augmented cellular uptake of (125)I-tyraminylcellobiose ox-LDL in JAR cells incubated with 8-iso-PGF(2alpha) (10 micromol/L) versus control cells. Ligand blots revealed an increased binding of ox-LDL to LOX-1 in JAR cells incubated with 8-iso-PGF(2alpha) (10 micromol/L). Incubation with 8-iso-PGF(2alpha) (10 micromol/L) also resulted in augmented LOX-1 protein levels (Western blots) and mRNA levels (Northern blots). JAR cells transfected with 3 copies of a nuclear factor-kappaB binding site demonstrated dose-dependent activation of the reporter gene luciferase after incubation with 8-iso-PGF(2alpha) (0 to 10 micromol/L). We also demonstrated increased accumulation of neutral fats in JAR cells incubated with 8-iso-PGF(2alpha) (10 micromol/L) and ox-LDL compared with controls by oil red O staining. We speculate a potential role of isoprostanes and LOX-1 in preeclampsia in the development of "acute atherosis" of gestational spiral arteries.

Azo Compounds↗

PubMed2000

Altered circulating levels of adhesion molecules at 18 weeks' gestation among women with eventual preeclampsia: indicators of disturbed placentation in absence of evidence of endothelial dysfunction?

OBJECTIVE: The purpose of this study was to investigate whether indications of activation of the maternal endothelium were present at 18 weeks' gestation in women in whom preeclampsia eventually developed. STUDY DESIGN: A total of 2190 blood samples were obtained at 18 weeks' gestation. Circulating levels of von Willebrand factor and soluble vascular adhesion molecule 1, soluble intercellular adhesion molecule 1, and E-selectin were assayed in 71 women with eventual preeclampsia and 71 control subjects. RESULTS: E-selectin and von Willebrand factor levels were similar between the 2 groups. Soluble vascular adhesion molecule 1 concentration was significantly lower in the women with eventual preeclampsia (median, 649.0 ng/mL vs 762.4 ng/mL; P <.001), whereas soluble intercellular adhesion molecule 1 concentration was significantly higher (median, 239.8 ng/mL vs 178.3 ng/mL; P <.001). CONCLUSION: We found no indications of endothelial activation at 18 weeks' gestation in women in whom preeclampsia later developed. However, decreased serum concentration of soluble vascular adhesion molecule 1 and increased serum concentration of soluble intercellular adhesion molecule 1 may reflect the disturbed placentation known to be associated with the development of preeclampsia.

Birth Weight↗

PubMed2000

The role of lipid oxidation and oxidative lipid derivatives in the development of preeclampsia.

Preeclampsia develops as a consequence of an exceptionally complex interaction between a multiplicity of factors that originate in 2 genetically different individuals (the mother and the fetus). Oxidative stress/oxidative lipid derivatives may represent one group of such factors. The evidence for a role of oxidative stress/oxidative lipid derivatives in the pathogenesis of preeclampsia may be summarized as follows: In women with established preeclampsia there is good evidence of increased oxidative stress/oxidative lipid derivatives in the decidual-placental tissues. Likewise, in the systemic circulation of women with established preeclampsia most of the studies although not all, indicate elevated levels of oxidative lipid derivatives and reduced anti-oxidative capacity. Because almost all studies on the role of oxidative stress in the pathogenesis of preeclampsia have been among women with established preeclampsia, it remains uncertain whether enhanced oxidative stress is present before clinical signs of preeclampsia develops. One controlled randomized study in which antioxidants were used to treat severe preeclampsia showed nonsignificant differences in clinical outcomes in favor of antioxidants. Controlled studies on the effectiveness of antioxidants in preventing preeclampsia are lacking. Such studies are of major interest in order to evaluate more definitely the role of oxidative stress/oxidative lipid derivatives in the pathogenesis of preeclampsia.

Female↗

PubMed2000

8-Iso-prostaglandin f(2alpha) reduces trophoblast invasion and matrix metalloproteinase activity.

Preeclampsia is a common pregnancy complication in the latter half of gestation diagnosed by hypertension and proteinuria. A key feature of preeclampsia is an altered placentation with reduced trophoblast invasion. Normal placentation requires controlled invasion of trophoblasts into the maternal uterine wall, with secretion of specific proteolytic enzymes able to degrade basement membranes and extracellular matrix, such as the matrix metalloproteinases (MMPs). 8-Iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)) is a marker of oxidative stress in vivo and is biologically active. We have recently reported an elevated content of free 8-iso-PGF(2alpha) in preeclamptic gestational tissue at delivery. Assuming an elevated level of 8-iso-PGF(2alpha) during the invasion period of the pregnancy, we hypothesized that 8-iso-PGF(2alpha) could reduce invasion of JAR cells, a choriocarcinoma cell line. We investigated JAR cell invasion with 2 types of Transwell assays and demonstrated that 8-iso-PGF(2alpha) (10 micromol/L) resulted in reduced cell invasion in both the colorimetric and radioactivity Transwell assays (P<0.01). Zymograms revealed reduced MMP-2 and MMP-9 activity in conditioned media from JAR cells incubated with 8-iso-PGF(2alpha) (10 micromol/L) (P<0.02). 8-Iso-PGF(2alpha) (10 micromol/L) also reduced the collagenase type IV activity in the conditioned media of JAR cells (P=0.04). No effects on MMP-2 and MMP-9 mRNA levels were observed after incubation with 8-iso-PGF(2alpha) (10 micromol/L), whereas protein levels were significantly decreased (P<0.02), suggesting a posttranscriptional regulation. We hypothesize a potential role for 8-iso-PGF(2alpha) in the reduced trophoblast invasion in preeclampsia.

Blotting, Western↗

PubMed1999

[Eclampsia].

Explore the source record for details and available documents.

Anticonvulsants↗

PubMed1999

Elevated level of free 8-iso-prostaglandin F2alpha in the decidua basalis of women with preeclampsia.

OBJECTIVES: The prostaglandin-like compound 8-iso-prostaglandin F(2alpha) represents an index of oxidative stress and has the ability to induce endothelial derangement, platelet activation, and vasoconstriction. In women with preeclampsia the decidual spiral arteries contain lipid deposits (acute atherosis). Analogously to the elevated level of 8-iso-prostaglandin F(2alpha) demonstrated in atherosclerotic lesions, we hypothesized that 8-iso-prostaglandin F(2alpha) level would be elevated in preeclamptic decidua basalis tissues. STUDY DESIGN: Decidua basalis tissues were obtained by vacuum aspiration and placental tissues were obtained by excision at cesarean delivery from 16 preeclamptic and 15 normal pregnancies. Total and free 8-iso-prostaglandin F(2alpha) concentrations were quantified with an enzyme immunoassay technique after lipid extraction and separation. RESULTS: The content of free 8-iso-prostaglandin F(2alpha) in preeclamptic decidual tissues was found to be significantly elevated with respect to that in control tissues. The content of total 8-iso-prostaglandin F(2alpha) did not differ significantly between the groups in either placenta or decidua basalis. CONCLUSIONS: We propose that free 8-iso-prostaglandin F(2alpha) released from the decidua basalis in preeclampsia may mediate maternal vascular dysfunction and platelet activation.

Adult↗

PubMed1999

Increased contents of phospholipids, cholesterol, and lipid peroxides in decidua basalis in women with preeclampsia.

OBJECTIVES: Accelerated recovery from preeclampsia has been reported after postpartum curettage. Lipid deposition in decidual spiral arteries (acute atherosis) is a histologic feature of preeclampsia. Increased tissue content of lipids is associated with enhanced formation of lipid peroxides, which are compounds that may induce endothelial dysfunction. We hypothesized that the content of lipids and lipid peroxides is elevated in decidua basalis tissues of women with preeclampsia compared with those of women with uneventful pregnancies. STUDY DESIGN: Decidua basalis tissues were obtained with a vacuum aspiration technique during cesarean delivery from 30 preeclamptic and 34 uneventful pregnancies. Total cholesterol, phospholipids, triglycerides, free fatty acids, and lipid peroxides were quantified. RESULTS: Significantly elevated contents of phospholipids, total cholesterol, and lipid peroxides were found in preeclamptic decidua basalis tissues, whereas the contents of triglycerides and free fatty acids did not differ significantly from those of the control group. CONCLUSIONS: Decidua basalis tissues, with their elevated lipid content, may be a source of lipid compounds that can cause maternal endothelial dysfunction in preeclampsia.

Adult↗

PubMed1999

Endothelial degradation of extracellular lyso-phosphatidylcholine.

Formation of lysophospholipids, including lyso-phosphatidylcholine (lysoPC), is enhanced during oxidation of low-density lipoprotein, in ischaemic tissue and under inflammatory conditions. Besides being potentially cytotoxic, extracellular lysoPC induces changes in several properties of vascular endothelial cells. These include expression of endothelial adhesion molecules and interference with the endothelial production of nitrogen monoxide, prostacyclin and growth factors. One way of controlling the concentration of extracellular lysoPC is by the action of lysophospholipases, which degrade lysoPC into a free fatty acid and glycerophosphocholine. We therefore tested whether vascular endothelial cells have the ability to degrade extracellular lysoPC. Monolayers of primary cultures of human umbilical vein endothelial cells degraded an average of 84+/-24 nmol lysoPC/10(6) cells/2 h. By comparison, monocytes degraded 9.7+/-3.7 nmol lysoPC/10(6) cells/2 h, and erythrocytes and platelets < 1 nmol lysoPC/10(6) cells/2 h. The ability of endothelial cells to degrade extracellular phospholipids (diacylphosphatidyl choline) was found to be relatively low (9.5+/-6.4 nmol/10(6) cells/2 h). Triacylglycerol hydrolase activity was just above detection level. In conclusion, endothelial cells seem to degrade extracellular lysoPC effectively. This endothelial property may be important in controlling plasma and tissue levels of extracellular lysoPC as well as in the interaction between lysoPC and the vascular endothelium.

Carbon Radioisotopes↗

PubMed1999

Foetal nutrition, foetal growth restriction and health later in life.

Retarded intrauterine growth has been linked to increased risk of perinatal mortality and morbidity, sudden infant death and poorer health later in life. The independent variables used in these studies are mainly neonatal size parameters, such as weight, ponderal index and ratios of head and abdominal measures. These are, in terms of foetal development and growth, crude parameters. This paper discusses the concepts of growth retardation used in most clinical and epidemiological studies. It is again emphasized that small for gestational age (SGA) and intrauterine growth retardation (IUGR) are different concepts. SGA is a size parameter that may or may not reflect restricted foetal growth and is therefore of limited value. Even IUGR, defined as retarded foetal growth rate, may be a too crude a criterion to select foetuses with short- and long-term health risks. Other biophysical measurements, such as foetal blood flow patterns and biochemical parameters, may be helpful in a better selection of these foetuses and infants. Furthermore, different causes of IUGR, e.g. poor maternal nutrition versus insufficient placental function, may not have the same effects on the foetus. The discrepancies in the results of studies on the relationship between IUGR or foetal malnutrition and short- and long-term health risks may be explained by the crudeness of the independent variables used. In the future, research on the biology of the developing human foetus should be more focused in the studies of the relationship between the intrauterine environment and nutrition and risk of poor health later in life.

Child Development↗

PubMed1998

[Intrauterine nutrition].

Foetal or intrauterine nutrition is a subject of increasing interest. There are two main reasons for this. The first one is the observation that being born small for gestational age is associated with increased risk of cardiovascular disease and diabetes later in life. The second one is the discovery that nutritional factors directly influence activity of genes. If nutritional inadequacies in the foetal period permanently alter the expression of genes, the individual's susceptibility to perinatal complications and diseases later in life may be altered. The main causes of intrauterine malnutrition are poor maternal diet, placental insufficiency, and impaired foetal usage of nutrients. The consequences of foetal malnutrition may include intrauterine growth retardation, congenital malformation, a variety of neurological dysfunctions, susceptibility to birth asphyxia, and diseases later in life; all of these are important determinants of health throughout life.

Birth Weight↗

PubMed1998

[Pregnancy, essential hypertension and chronic renal disease].

Women with chronic hypertension or renal disease are at a particular high risk of developing pre-eclampsia or eclampsia. Pre-eclampsia is associated with an increased risk of fetomaternal complications. In women with uncomplicated mild and moderate hypertension, pregnancy is usually normal. Treatment of high blood pressure aims at reducing maternal cardio- and cerebrovascular catastrophies, and the benefit of the treatment must be weighed against possible harmful effects on the foetus. In some cases, antihypertensive treatment can be discontinued, or medication changed. Preconceptional counselling is important both for women with chronic hypertension and, even more so, for women with renal disease, since the outcome of the pregnancy may be affected by the underlying disease.

Female↗

PubMed1998

[Measurement of blood pressure in pregnancy].

The prevalence of hypertension in pregnancy is 4-10 percent. The most serious complication associated with hypertension in pregnancy is pre-eclampsia. In one out of ten pregnancies where pre-eclampsia is present very serious complications develop in the mother or the foetus, or both. Rising blood pressure remains the main indicator of impending pre-eclampsia. The reliability of blood pressure measurement is therefore of particular importance in pregnancy. This is emphasized by the following characteristics of hypertension in pregnancy: limited time to observe the patient; pre-eclamptic complications may be present at any stage where there is a rise in blood pressure, and the indications for and objectives of treatment of pregnancy hypertension are different from those employed in the general population. The measurement of antenatal blood pressure should be standardized. It should be carried out by a limited number of well-qualified health professionals, using only equipment of reknowned quality and technical standard. Rising blood pressure in pregnancy indicates pre-eclampsia until it has been disproved post partum. Because pre-eclampsia is a placental disorder, the foetus may be at risk at any stage in the development of the disease. The status of the foetus should therefore be monitored accordingly.

Blood Pressure Determination↗

PubMed1998

Plasma lipids and vascular dysfunction in preeclampsia.

The dominating hypothesis of the preeclampsia syndrome (PES) is that placentally derived factors are released to the maternal circulation. These factors are believed to alter endothelial properties resulting in disturbed vasomotor function, increased endothelial permeability, and activation of thrombogenic factors. However, the impact of placentally derived factors on the endothelial cells is influenced by another major variable: the "sensitivity" of the maternal endothelium to the placental factors. Several maternal factors may play a role in determining this sensitivity. They include chronic hypertension, diabetes, and hyperlipidemia. In this article we discuss the possible role of hyperlipidemia (especially high free fatty acids and hypertriglyceridemia) in the pathogenesis of preeclampsia, viewed from this perspective. Pregnancy in general, preeclamptic pregnancy in particular, is associated with a marked hyperlipidemia. We suggest a parallel to atherosclerotic diseases, wherein hyperlipidemia induces endothelial dysfunction, probably by promoting oxidative stress in the arterial wall. The hyperlipidemia of pregnancy may have a similar effect on the endothelial cells. When placentally derived endothelial disturbing factors, like lipid peroxides and trophoblastic components, are released into the maternal circulation, their effects on the endothelium may be enhanced because of hyperlipidemia-mediated activation or "sensitization" of the endothelial cells. Alternatively, placentally derived factors like peroxides may combine with lipoproteins, forming complexes that are more disturbing to cells than the placental factors or lipoproteins are individually. We also discuss the possible role of maternal hyperlipidemia in aggravating placental insufficiency caused by poorly transformed spiral arteries. The hemodynamic flow pattern may be markedly different in completely and incompletely transformed spiral arteries. By analogy to the fundamental role of hemodynamic factors in development of atherosclerosis, we pose the hypothesis that abnormally transformed spiral arteries have an "atherogenic" blood flow pattern that promotes lipid deposition and "acute atherosis".

Arteriosclerosis↗

PubMed1998

Glucose intolerance in women with preeclampsia.

BACKGROUND: We have previously shown that women with proteinuric hypertension of pregnancy (preeclampsia) have increased circulating levels of triglycerides and free fatty acids. Preeclampsia has, therefore, several features in common with the insulin resistance syndrome. The objective of the present study was to investigate the glucose tolerance and insulin response of women with preeclampsia compared to women with normal pregnancy. METHODS: Oral glucose tolerance test was performed in ten women with preeclampsia and eight healthy women with normal pregnancy. The glucose, insulin, C-peptide and free fatty acid responses were calculated. RESULTS: The mean fasting glucose concentration was significantly lower in preeclamptic women (3.3 vs 3.7 mmol/l; p = 0.02). Fasting serum triglycerides were increased in women with preeclampsia compared to normal pregnancy (3.3 vs 1.9 mmol/l; p = 0.003). Women with preeclampsia had also increased serum free fatty acids, 0.52 vs 0.36 mmol/l for normal pregnancy; p = 0.056). Log s-insulin and cholesterol were not different. The incremental area under the curve for the glucose (p = 0.001) and insulin (p = 0.02) responses to oral glucose tolerance test showed higher values for preeclampsia as compared to women with normal pregnancy. For free fatty acids the total area under the suppression curve was higher in women with preeclampsia (p = 0.03). CONCLUSIONS: These results support the concept that preeclampsia is associated with metabolic aberrations found in insulin resistance syndrome.

Adult↗

PubMed1998

Hypertension in pregnancy and preeclampsia--diagnosis and treatment.

Women who have or develop high blood pressure during pregnancy are all at increased risk of complications antenatally, intrapartum and in the puerperium. The increased risk applies to the mother as well to the fetus. Preeclampsia is the most serious form of hypertensive pregnancy complications. Preeclampsia is, however, not primarily a hypertensive disease but a disorder induced by factors dependent on the presence of placenta. The prime target of the placenta dependent factors is the vascular endothelium. Therefore the complications are associated with the vascular system, i.e. intravascular coagulation, bleeding and organ failure following poor perfusion. The fetus is at increased risk due to growth retardation and hypoxia following placental damage. Treatment of the hypertension is first indicated if the blood pressure rises to a level of increased risk of cerebral vascular complications, i.e. above 105-110 mmHg. Delivery is the only causal treatment and is always indicated if severe maternal or fetal complications develop.

Female↗