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Biomedical subjects

H Jansen

Publications and source records attributed to H Jansen.

At least 145 records · Page 8Linked to original sources
PubMed1987

Diet and the role of lipoproteins, lipases, and thyroid hormones in coronary lesion growth.

Relationships between lipoprotein fractions, lipoprotein lipase activities, thyroid hormones, and coronary lesion growth were studied among 35 male patients with severe coronary atherosclerosis, who had participated in the Leiden Intervention Trial, a lipid-lowering dietary intervention program. Coronary arteriography was performed at the beginning of the study and again 2 years later at its termination. The lesions were quantified using a computer-based analysis system to assess the progression rate of coronary lesions based on absolute arterial dimensions in a patient's coronary tree. For this reason an absolute coronary score was computed. Based on absolute coronary scores, patients could be divided into a no-lesion growth group (14 patients) and a progression group (21 patients). Lipoprotein fractions, lipoprotein lipases, and thyroid hormones were determined at the end of the trial. No significant differences were found between the no-lesion growth and progression groups for total cholesterol and low-density lipoprotein (LDL) cholesterol. In the progression group very-low-density lipoprotein (VLDL) cholesterol and triglycerides were significantly higher (p less than 0.05) and high-density lipoprotein (HDL) cholesterol was almost significantly lower (p = 0.058). Hepatic lipase (HL) values were significantly higher in the no-lesion growth group, when compared with the progression group, whereas lipoprotein lipase (LPL) values were not significantly different. Triiodothyronine (T3) was significantly lower (p less than 0.01) in the progression group. Multivariate regression analysis showed HL to be the most important determinant of changes in coronary atherosclerotic lesions. T3 and HDL cholesterol were also independently inversely related to coronary lesion growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Parallel column ion exchange for post-separation pH modification in liquid chromatography. Application to barbiturates and miniaturization.

A new approach to the UV detection of barbiturates in high-performance liquid chromatography is demonstrated. The analytical system comprises an anion-exchange column inserted parallel to the injection valve and analytical column. One part of the acetate-containing mobile phase flows through the injection valve and analytical column to achieve the separation, the other part flows through the anion-exchange column where the acetate ions cause the release of hydroxide ions from this column. Finally, the alkaline stream from the anion-exchange column is recombined with the analytical column effluent. This results in an alkaline medium which can be favourable for many detection processes. A series of barbiturates, which show enhanced UV detectability at 254 nm in alkaline solution, was chosen to demonstrate the potential of such a method. Applications of this principle to the analysis of urine and plasma samples are described. In the system only one pump is needed for the separation and the post-column pH modification. A critical comparison between conventional scale and narrow-bore systems is made.

Barbiturates↗
PubMed1986

Human hepatoma (Hep G2) cultures contain salt-resistant triglyceridase ("liver lipase").

The culture fluid of Hep G2 human hepatoma cells contains triglyceridase activity resistant to high-salt concentrations. The lipase binds to Sepharose-heparin columns from which it can be eluted by 0.8 to 0.9 M NaCl. The nature of this lipase was studied using antibodies raised against "liver" lipases from human and rat origin. The anti-rat liver lipase inhibits both the postheparin human and rat plasma enzyme while the anti-human liver lipase has no effect on the rat enzyme. The lipase of the Hep G2 cultures showed affinity to the antibodies raised against rat as well as human "liver" lipase as shown by inhibition experiments. These results show that Hep G2 cells secrete "liver" lipase and that there seems to exist a structural homology between the lipases from rat and human origin.

Animals↗
PubMed1986

Monoclonal antibodies against salt-resistant rat liver lipase. Cross-reactivity with lipases from rat adrenals and ovaries.

To obtain monoclonal antibodies against rat salt-resistant liver lipase, mice were immunized with enzyme purified from heparin-containing rat liver perfusates. Hybridomas were screened for antibody production by means of an enzyme-linked immunosorbent assay (ELISA) and an immunoprecipitation assay. Five hybridoma cell lines secreting antibodies against rat liver lipase indicated as A, B, C, D and E, have been obtained. All antibodies possess gamma one (gamma 1) heavy chains and kappa (kappa) light chains. The antibodies precipitate salt-resistant lipase from rat post-heparin plasma, are positive in ELISA, inhibit liver lipase activity and bind monospecifically with the enzyme as shown by immunoblotting. The monoclonal antibodies showed no significant reactivity with human liver lipase. The salt-resistant lipases of rat adrenals and ovaries are also precipitated by the monoclonal antibodies directed against the liver enzyme. Therefore, the heparin-releasable lipases of the liver, adrenals and ovaries possess identical epitopes.

Adrenal Glands↗
PubMed1986

[Echography of the normal kidney in infants].

In 33 infants from 0 to 11 months old, apparently without urinary tract disease, the kidneys were examined sonographically. Renal length was correlated with age and bodyweight. The renal echopattern was studied: Normal kidneys in newborn and young infants have several distinct sonographic features: the renal cortex is more echogenic, the medullary pyramids are prominent and relatively anechoic, the central sinus echo is reduced. This pattern occurs until the age of 3 months and changes to the adult pattern at the age of 5 months.

Aging↗
PubMed1985

Inhibition of liver lipase in vivo leads to induction of de novo cholesterol synthesis in rat liver.

Rats were injected with control-gamma-globulins or anti-liverlipase. The anti-liverlipase treatment resulted in a 69-78% inhibition of the salt-resistant lipase activity (liver lipase) in the liver. De novo cholesterol synthesis was significantly higher in slices of livers from anti-liverlipase treated rats than from control-gamma-globulin injected rats. The anti-liverlipase treatment also affected all plasma lipoprotein fractions. If the rats had been fed a cholestyramine containing diet no effect of anti-liverlipase on cholesterol synthesis was found. In these rats the effects on plasma lipoprotein fractions were more pronounced than in the control fed rats.

Animals↗
PubMed1985

Diurnal changes in serum triglycerides as related to changes in lipolytic enzymes, lipoproteins and hormones in patients with primary endogenous hypertriglyceridaemia on a carbohydrate-rich diet.

Parameters of diurnal triglyceride (TG) metabolism were investigated in 5 subjects with primary endogenous hypertriglyceridaemia and compared with those of normal subjects studied previously. The patients were in a steady state on a carbohydrate-rich diet (meals at 9.00, 13.00 and 17.00 h). Serum TG showed a wavelike pattern with a maximum at around 17.00 h. Post-heparin lipoprotein lipase (LPL) activity in the fasting state was not different from that in normals, but failed to show the normal increase in the fed state (16.30 h). This was due to the inability of patients to increase their adipose tissue (AT)-LPL activity in the course of the day. AT-LPL activity was throughout the day lower than in normal subjects. Skeletal muscle LPL activity was low and showed no diurnal change, equalling our findings in normal subjects. Low density lipoprotein cholesterol and high density lipoprotein (HDL) cholesterol concentrations showed no diurnal change. However, HDL phospholipids increased significantly in the course of the day.

Adipose Tissue↗
PubMed1985

The effect of Synacthen administration on lipoprotein lipase activity in the epididymal fat pad of the rat.

Conflicting data have been reported on the influence of (excess) glucocorticoids on lipoprotein lipase (LPL) activity in adipose tissue. To solve this problem hypercorticism was induced in rats by treatment for varying periods with Synacthen, a synthetic corticotrophin-1-24 preparation, and LPL was measured in the epididymal fat pads using different methods. In extracts of defatted tissue preparations from overnight fasted rats treated for 3 days with Synacthen we observed an increase in LPL activity (acetone-ether powder LPL) to values similar to those found in normally fed controls. In contrast, the heparin-elutable part of LPL activity in the tissue was not influenced by the Synacthen treatment. This activity remained significantly lower in overnight fasted animals, Synacthen treated or not, than in normally fed rats. Adrenalectomy lowered the acetone-ether powder LPL activity of the epididymal adipose tissue in fasted as well as in fed rats. In fasted rats it prevented the stimulation of the LPL activity by Synacthen.

Adipose Tissue↗
PubMed1985

Localization of liver-type lipase in rat ovaries and its activity during the estrous cycle and lactation.

The conditions for an in vitro assay of liver-type lipase, i.e. an enzyme resembling the lipase releasable from the liver by heparin (liver lipase), in rat ovaries were established. The liver-type lipase activity in the ovaries was almost completely (greater than 95%) located in the corpora lutea and its activity ranged from 0.44 to 0.77 mU per corpus luteum of (pseudo)pregnant rats. Preovulatory ovarian follicles contained very low lipase activity. During the estrous cycle the pattern of lipase activity was similar to that of serum progesterone levels (maximal at diestrus 1 and minimal at diestrus 2). In the individual rats liver-type lipase activity in the ovaries was strongly correlated with serum progesterone and 20 alpha-hydroxyprogesterone. The activity of liver-type lipase also varied during lactation. It was relatively low at an early stage (2-3 days) but increased during later stages of lactation. The serum progesterone level was relatively low in rats lactating for 2-3 or 22-24 days. During the intervening time, its concentrations was elevated. Since serum 20 alpha-hydroxyprogesterone levels varied inversely to progesterone, the total amount of progestagens in blood during lactation remained constant. The cholesterol content of the corpora lutea of the lactating rats was initially high and decreased during the lactation.

Animals↗
PubMed1985

[Comparative study of somatosensory evoked potentials, whole body computer tomography and myelography in spinal space-occupying lesions].

Somatosensory evoked potentials (SEP) of the tibial nerve are of diagnostic value, if the recording points nearest to the spinous process are used. In cases with space-occupying lesions of the spinal cord, conduction block or amplitude reduction is the most common abnormality. In contrast in inflammatory diseases like spinal MS the most common abnormality is marked latency delay.

Evoked Potentials, Somatosensory↗
PubMed1984

Regulation of liver lipase. II. Involvement of the alpha 1-receptor.

The effects of different adrenergic agents on high density lipoprotein (HDL) cholesterol concentration and on the neutral NaCl-resistant triacylglycerol hydrolase (liver lipase) activity of the liver were studied in rats. Treatment of rats with the beta-blockers metoprolol, atenolol or propranolol led to a lowering of the HDL-cholesterol (esterified and non-esterified) content. The alpha 1-antagonist prazosin had no effect. Administration of norepinephrine for 10 days resulted in an increase of HDL non-esterified cholesterol. This effect of norepinephrine was largely abolished by prazosin, but not by propranolol. In normal rats the liver lipase activity was not influenced by alpha- or beta-blockade. Adrenergic stimulation, either short-term (by diethyl ether stress) or long-term (by norepinephrine treatment), led to a lowered liver lipase activity. The lipase activity was restored by prazosin but not by propranolol. The apparent involvement of the alpha 1-receptor in the regulation of liver lipase activity was further studied in vitro. Blockade of alpha- or beta-receptors with prazosin or propranolol did not affect the secretion of the liver lipase activity by isolated parenchymal liver cells. Stimulation of alpha- or beta-receptors by epinephrine led to a lower secreted lipase activity. Selective stimulation by isoprenaline had no effect. The effect of epinephrine could be abolished by prazosin but not by propranolol. Vasopressin and the calcium ionophore A23187 also lowered the secretion of liver lipase activity in vitro. Glucagon and/or the phosphodiesterase inhibitor Ro 20-1724 had no effect. These results indicate an involvement of the alpha 1-receptor in the regulation of liver lipase activity at the level of synthesis or secretion of the lipase. The effect of the alpha 1-receptor is presumably mediated through changes in the intracellular free calcium concentration. The effect of adrenergic modulation on HDL-cholesterol concentrations can partly be explained through modification of the liver lipase activity.

Adrenergic beta-Antagonists↗
PubMed1984

Effect of low-dose oral contraceptives on lipoproteins and lipolytic enzymes: differences between two commonly used preparations.

Changes in circulating lipoproteins, which may be related to the risk for atherosclerotic vascular disease, were studied in a control group and in two groups of 24 or 26 women using different preparations of low-dose oral contraceptives for 3 months. One preparation contained 150 micrograms levo-norgestrel and 30 micrograms ethinylestradiol (Stediril-d 150/30); the other contained 750 micrograms lynestrenol and 37.5 micrograms ethinylestradiol (Ministat). No significant changes were found with either of the preparations in serum cholesterol or high density lipoprotein cholesterol (HDL-C) levels. Apolipoprotein A-II levels increased during Ministat treatment from 50.4 to 61.4 mg/dL and during Stediril-d 150/30 treatment from 52.7 to 58.9 mg/dL (both P less than 0.001). These changes differed significantly from each other (P less than 0.01). Apolipoprotein A-I levels increased significantly during use of Ministat only. Apolipoprotein B in low density lipoprotein increased by about 20% (P less than 0.001) in both groups. Post-heparin lipoprotein lipase activity did not change, but hepatic lipase activity decreased to the same extent in both groups (P less than 0.001). Reductions in post-heparin lipase activity were not correlated with increases in HLD-C.

Adult↗