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Biomedical subjects

P Holck

Publications and source records attributed to P Holck.

17 recordsLinked to original sources

[Henrik Wergeland's disease and death. 150th anniversary].

It is 150 years since the Norwegian poet Henrik Wergeland (1808-45) died. It is commonly assumed that the suffered from "phthisis" or--as we now call it--tuberculosis. This paper discusses the symptoms mentioned in Wergeland's own letters, which seem to indicate that the diagnosis was instead pulmonary cancer.

Diagnostic Errors

[From the early history of cancer treatment].

Skeletal finds have shown that tumorous diseases are as old as mankind itself. However, the appearance of such diseases have been rather differently understood, explained and treated throughout the history of medicine. This paper gives a brief survey of the development of cancer treatment and research, in Norway and in the other European countries.

Europe

Effect of needle biopsy from the vastus lateralis muscle on insulin-stimulated glucose metabolism in humans.

To examine the cellular mechanisms behind conditions characterized by insulin resistance, the clamp technique is often combined with muscle biopsies. To test whether the trauma of a needle biopsy from the vastus lateralis muscle per se may influence insulin-stimulated glucose uptake, eight healthy subjects underwent two randomly sequenced hyperinsulinemic (insulin infusion rate: 0.6 mU.kg-1.min-1 for 150 min) euglycemic clamps with an interval of 4-6 wk. In one study (study B) a muscle biopsy (approximately 250 mg, i.e., larger than normal standard) was taken in the basal state just before the clamp procedure, whereas the other was a control study (study C). Insulin-stimulated glucose uptake was significantly reduced in study B (5.36 +/- 0.96 mg.kg-1.min-1) compared with study C (6.06 +/- 0.68 mg.kg-1.min-1; P < 0.05). Nonoxidative glucose disposal (indirect calorimetry) was decreased (2.81 +/- 1.08 vs. 3.64 +/- 1.34 mg.kg-1.min-1; P < 0.05), whereas glucose oxidation was unaltered. Likewise, endogenous glucose output ([3-3H]glucose) was identically suppressed during hyperinsulinemia. Circulating levels of epinephrine, glucagon, and growth hormone did not differ significantly in studies B and C. In contrast, plasma norepinephrine, serum cortisol, and free fatty acid rose after biopsy (P < 0.05). In conclusion, performance of a muscle biopsy may diminish insulin sensitivity by affecting nonoxidative glucose metabolism. This should be considered when assessing whole body insulin sensitivity after a percutaneous needle muscle biopsy.

Adult

[The Bartholinian era--anatomy at the time of Christian IV].

At the time of King Christian IV of Denmark and Norway the University of Copenhagen was one of the most famous universities in Europe because of the epoch making medical research carried out there. The author presents a dynasty of anatomists--the Bartholin family--who dominated medical teaching and science for a century.

Anatomy

Structure and segmental localization of glycogen in the diabetic rat kidney.

Pathological accumulations of glycogen were studied in the kidney tubular epithelium in untreated STZ-induced diabetic rats of 50 days diabetes duration. Blood glucose concentrations were approximately 17 mM, and the animals had no ketonuria. At the termination of the experiment, the kidneys were perfusion-fixed, and serial sections were cut from the renal capsule to the tip of the papilla and stained with toluidine blue and periodic acid Schiff. By tracing tubular profiles from section to section in a light microscope, the outlines of nephrons were reconstructed, and abnormal glycogen accumulations were mapped in accordance with the outlines. The exact segmental localization, character, and extension of the glycogen accumulations were determined. The predominant location of the pathological glycogen accumulations was in the thick ascending limb of Henle's loop. Dot-shaped and diffuse-appearing glycogen accumulations were discretely distributed throughout the segment, and large confluent cytoplasmic accumulations of glycogen were also present. On a continuous basis, glycogen was present only in the cortical thick ascending limb of Henle's loop and the macula densa segment excluding the macula densa cells. In the distal convoluted tubule and the cortical collecting duct system, scattered dot-shaped and diffuse glycogen accumulations were discretely distributed. Furthermore, glycogen appeared as confluent, cytoplasmic accumulations in the initial part of the descending thin limb of Henle's loop. In addition, glycogen accumulations were found in nuclei within a narrow stripe of the outer stripe of the outer medulla in the medullary thick ascending limb of Henle's loop.

Animals

Fixation of the macula densa with fixatives of different osmolarities in normal and diabetic rats.

The influence of different fixative osmolarities on the ultrastructure of the macula densa region has been studied in normal and in streptozotocin diabetic rats after 50 days' duration of diabetes. In vivo perfusion fixation of the kidneys was performed retrogradely through the aorta in five groups of controls and diabetic animals with a 1% glutaraldehyde fixative in a Tyrode solution. Between groups, the osmolarity of the fixative solution varied from 216 to 476 mosm/l. This was accomplished by variation of the NaCl concentration of the fixative vehicle. The tissue was embedded in Epon and midcortical tissue was prepared for electron microscopy. The volume density of the lateral intercellular spaces between the macula densa cells was measured applying a morphometric technique. The results confirmed that the lateral intercellular spaces are narrowed in diabetes and also showed that for all fixative osmolarities the difference is persistent between diabetic and non-diabetic animals, except at very low osmolarities. The abnormal macula densa ultrastructure has been suggested to be connected with the functional abnormalities in diabetes, i.e. the resetting of the tubuloglomerular feedback and subsequent increases in GFR. It is therefore of interest to further understand the mechanisms underlying the narrowing of the lateral intercellular spaces in diabetes. The present study has shown that the size difference in lateral intercellular spaces between diabetic and normal animals is reproducible over a wide range of fixative osmolarities, further indicating that it is an in vivo phenomenon. The diminution of the LIS in diabetes could perhaps indicate a decrease in signal function, previously reported at the MD level in diabetic animals, contributing to the increased GFR in diabetes.

Animals

Macula densa morphology in diabetic rats with and without hyperglycemia and in nondiabetic hyperglycemic rats.

The morphology of the macula densa was studied in streptozotocin diabetic insulin-treated rats with hyperglycemia for 50 days, and in three groups of diabetic rats that were first hyperglycemic for 50 days and then put onto different insulin regimes to achieve normoglycemia. One of the latter groups of rats was given a single dose of insulin and was studied 4 hours later when the animals were normoglycemic. The other two groups were treated with insulin for 5 and 15 days in such a way that the animals were nearly normoglycemic throughout the treatment period. In a further set of experiments two groups of nondiabetic rats were made hyperglycemic by intravenous injection of glucose and studied after 1 and 10 minutes of hyperglycemia. A perfusion fixation of the kidneys was performed in all animals with a 1% glutaraldehyde solution retrograde through the aorta, and the tissue was embedded in Epon for light and electron microscopy. Juxtaglomerular apparatuses were randomly selected from thick sections and reembedded for electron microscopy. The volume density of the lateral intercellular spaces (LIS) between the macula densa cells was determined on electron micrographs, by use of a morphometric technique. The study showed that the volume density of the LIS comprised about 10% in the nondiabetic normoglycemic animals and about 1.5% in the diabetic hyperglycemic animals. In all the insulin-treated normoglycemic diabetic animals, the volume density of the LIS was the same as in the nondiabetic normoglycemic animals (about 10%), independent of the duration of the insulin treatment. In the nondiabetic hyperglycemic animals the volume density of the LIS comprised about 1.5%, as in the diabetic hyperglycemic animals. In conclusion, the volume density of the LIS between the macula densa cells is reduced in a hyperglycemic state, irrespective of how the hyperglycemia was achieved, and they are normalized (i.e., enlarged) in insulin-treated diabetic normoglycemic animals irrespective of the duration of the treatment. The results indicate that changes in the blood glucose concentration have a major impact on the size of the macula densa LIS.

Animals

[From the history of brain research].

This paper describes the understanding of the brain and central nerve system from antiquity up to our own century. It also describes the first attempts at brain research in the Nordic countries, and in Norway in particular.

Animals

[Asbestos in the work environment. The occurrence of pulmonary changes among workers exposed to asbestos at an electrotechnical factory].

A number of workers exposed to asbestos dust for more than three months were medically examined for lung diseases caused by asbestos. A follow-up examination four years later revealed that the lung capacity of these workers was significantly lower than in the normal population. 9% of them showed changes in the lungs caused by asbestos dust, but no case of cancer was discovered. There was no development of significance in these changes during the four years.

Adult

Ultrastructure of the macula densa in streptozotocin diabetic rats.

Morphometric analyses of the macula densa in streptozotocin diabetic rats have revealed, that the volume density of the large lateral intercellular spaces, which are present in normal animals between the macula densa cells, decreases significantly in magnitude from 8.7 to 1.5% in diabetic animals. The volume density of cytoplasmic glycogen in the macula densa cells increases significantly from 5.4% in the controls to 14.8% in the diabetic animals, but the total volume density of mitochondria is the same in the two groups. The contact area between macula densa cells and the Goorgmaghtigh cells is increased by 38% in the diabetic animals compared with controls. The structural abnormalities in the macula densa in response to diabetes might be considered a structural counterpart to the alterations in the tubuloglomerular feedback mechanism and the increase in glomerular filtration rate in diabetes.

Animals