Biomedical subjects
T Henriksen
Publications and source records attributed to T Henriksen.
[Laparoscopy in infertility. A comparison of findings and treatment].
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[Gonadotropin releasing hormone agonists. A new therapeutic principle in gynecology].
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[Gamete intrafallopian transfer in infertility].
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[In vitro fertilization].
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Pregnancies after intrafallopian transfer of embryos.
Six patients with a history of infertility of more than 4 years were offered in vitro fertilization (IVF) followed by translaparoscopic embryo transfer to the fallopian tubes. Three of the patients became pregnant. In one patient the oocytes did not fertilize in vitro. Intrafallopian transfer of embryos may be an alternative to gamete intrafallopian transfer (GIFT) or IVF, especially in those cases where confirmation of fertilization is wanted.
Oocyte retrieval in an IVF program. A comparison of laparoscopic and transvaginal ultrasound-guided follicular puncture.
From 1 April 1986 to 20 May 1987, 160 oocyte retrievals were performed in our IVF program. 80 oocyte retrievals were done by laparoscopy under general anaesthesia and 80 under light sedation and local analgesia using transvaginal ultrasound guided follicle puncture. More oocytes were recovered with the ultrasound procedure than with laparoscopy, 616 versus 478. The fertilization rate was higher when the oocytes were collected with the ultrasound procedure, vis-à-vis laparoscopy, 70.6% versus 59.6%. The number of embryos transferred was greater in the former than in the latter group, 300 versus 182. There were 13 clinical pregnancies in the laparoscopy group versus 17 in the ultrasound group. There were no serious complications in either group. Transvaginal ultrasound guided follicle aspiration is a safe and simple procedure.
Pregnancy after translaparoscopic embryo intrafallopian transfer (EIFT).
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Pregnancy after gamete intrafallopian transfer.
A couple with a history of 6 years' unexplained infertility was treated by gamete intrafallopian transfer (GIFT). Thus, oocytes were obtained by laparoscopy and immediately placed in a transfer catheter together with sperms. The oocyte/sperm preparation was injected into the Fallopian tube via a separate trochar under laparoscopic direction. Four weeks later pregnancy was confirmed by ultrasound.
Endocytosis of acetylated low-density lipoprotein, endothelial cell-modified low-density lipoprotein, and formaldehyde-treated serum albumin by rat liver endothelial cells. Evidence of uptake via a common receptor.
Formaldehyde-treated serum albumin (FSA) and acetylated low-density lipoprotein (Ac-LDL) are taken up in vivo and in vitro by the sinusoidal endothelial cells of the liver. It is not known whether both these ligands are removed by the scavenger receptor. We have studied the effect of increasing concentrations of unlabeled FSA, Ac-LDL, and endothelial cell-modified LDL (Ec-LDL) on the endocytosis of trace amounts of these ligands labeled with 125I. Uptake of 125I-Ac-LDL and 125I-Ec-LDL was strongly inhibited by FSA. Likewise, Ac-LDL and Ec-LDL reduced the uptake of 125I-FSA effectively. Our data indicate that these modified LDLs and FSA are bound to and internalized via the same receptor on liver endothelial cells.
Tissue uptake of biologically modified low density lipoprotein in the rat.
Human low density lipoprotein (LDL) was modified by exposure to cultured human endothelial cells. The endothelial cell modified LDL (EC-LDL) and control LDL (con LDL) labelled with 125I-tyramincellobiose (125I-TC) were injected into rats. Since 125I-TC is trapped in lysosomes the contribution of various organs to the catabolism of EC-LDL and con LDL could be studied. First, EC-LDL was cleared from plasma several times faster than con LDL. Then, the liver was found to be the major organ for catabolism of EC-LDL. Con LDL was distributed more evenly among the spleen, liver and adrenals as the main organs. In the liver the endothelial cells were most effective in degrading EC-LDL whereas con LDL was distributed approximately evenly between the Kupffer, endothelial and parenchymal cells. Thus, the liver endothelial cells seem to be a major pathway for catabolism of modified LDL.
[Plasma lipids and plasma lipoproteins].
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Oxidized low density lipoprotein can reduce the pinocytic activity in cultured human endothelial cells as measured by cellular uptake of [14C]sucrose.
The effect of low density lipoprotein (LDL) on the pinocytic activity in human endothelial cells in culture, as measured by the uptake of [14C]sucrose, was studied. The cells were preincubated for 48 h with a low concentration of LDL (25 micrograms protein/ml) or a high concentration of LDL (150 micrograms protein/ml) in the presence of lipoprotein deficient serum. Then the pinocytic activity of the cells was measured in a subsequent incubation by measuring the uptake of [14C]sucrose. The higher LDL concentration resulted in a reduced cellular uptake of [14C]sucrose compared to the lower concentration of LDL. When the additional LDL (the lower concentration subtracted from the higher) was replaced by high density lipoprotein, albumin or gamma globulin, no reduction of the uptake of [14C]sucrose was observed. The inhibitory effect of LDL on the uptake of [14C]sucrose was seen in endothelial cell cultures of different age and cell density. When the endothelial cell proliferation was arrested by gamma irradiation, the reducing effect of LDL on the pinocytic activity was unchanged as compared to nonirradiated controls. LDL prepared in the presence of EDTA and glutathione did not have the same reducing effect on the uptake of [14C]sucrose as control LDL prepared in the absence of antioxidants. Thus, oxidized LDL reduced the pinocytic activity in cultured endothelial cells. The inhibitory effect of LDL on the rate of pinocytosis was present before endothelial cell injury could be observed.
Interaction of human endothelial cells with elevated glucose concentrations and native and glycosylated low density lipoproteins.
We have investigated whether and how the elevated glucose concentrations characteristic of diabetes may alter the interaction of endothelial cells with low-density lipoproteins (LDL). Protracted exposure of cultured human endothelial cells to 20 mmol/l glucose failed to affect either the relationship between the degree of confluency of the monolayer and the extent of LDL degradation or the dose-responses for LDL uptake and degradation. In contrast, non-enzymatic glycosylation of LDL by pre-incubation of LDL with glucose markedly inhibited their uptake and degradation by endothelial cells. Thus, at protein concentration of 5 micrograms/ml, the amount of glycosylated 125I-LDL associated with cells was decreased fourfold compared with native 125I-LDL (47 +/- 3 versus 194 +/- 10 ng X mg cell protein-1 X 24 h-1, mean +/- SEM), and degradation was decreased twenty-fold (135 +/- 4 versus 2873 +/- 115 ng X mg cell protein-1 X 24 h-1). The degree of inhibition was proportional to the extent of glycosylation. At all concentrations studied, methylated LDL behaved similarly to glycosylated LDL. The decreased recognition of glycosylated LDL by the endothelial lining of small and large blood vessels may have an impact of tissue physiology and on the overall fate of the glycosylated molecules.
Possible biological mechanisms that make low density lipoproteins a risk factor in atherogenesis.
Low density lipoprotein (LDL) is a risk factor in the development of atherosclerosis. The biological mechanism for this association has been obscure. This paper shows that LDL can be modified in vitro by several chemical and biological means. Modified forms of LDL seem to make it susceptible to enhanced uptake in macrophages. LDL may also induce disturbance of the surrounding cells, especially endothelial cells, as it is potentially cytotoxic. An hypothesis is presented based on the fact that LDL is a labile lipoprotein and may, while situated in the arterial wall, undergo modifications and thereby lead to lipid deposition.
[A radiation accident with lethal outcome].
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[A radiation accident with fatal outcome].
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Dosimetry by ESR spectroscopy following a radiation accident.
On 2 September, 1982, one of the employees of the gamma-irradiation facility at The Institute for Energy and Technology (Kjeller, Norway) entered the irradiation cell with a 65.7-kCi 60Co source in unshielded position. The victim received an unknown radiation dose and died after 13 days. Using electron-spin resonance spectroscopy (ESR), the radiation dose in this accident was subsequently determined based on the production of long-lived free radicals in nitroglycerol tablets carried by the operator during accident. He used nitroglycerol for heart problems and free radicals are easily formed and trapped in sugar which is the main component of the tablets. Calibration experiments were carried out and the dose given to the tablets during the accident was determined to be 39 Gy. Phantom experiments based on this result indicate an average whole-body dose in the accident of 22.5 Gy.