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Biomedical subjects

F Carlsen

Publications and source records attributed to F Carlsen.

16 recordsLinked to original sources
PubMed1998

More physicians: improved availability or induced demand?

A number of empirical studies have shown that there is a negative association between population:physician ratio and utilization of medical services. However, it is not clear whether this relationship reflects supplier-inducement, the effect of lower prices on patient demand, a supply response to variation in health status, or improved availability. In Norway, patient fees and state reimbursement fees are set centrally. Therefore, the correlation between utilization and population:physician ratio either reflects supplier-inducement, a supply response or an availability effect. We applied a theoretical model which distinguished between an inducement and an availability effect. The model was implemented on a cross-sectional data set which contained information about patient visits and laboratory tests for all fee-for-service primary care physicians in Norway. Since population:physician ratio is potentially endogenous, an instrumental variable approach is used. We found no evidence for inducement either for number of visits or for provision of laboratory services.

Clinical Laboratory Techniques↗
PubMed1995

Supplier inducement in a public health care system.

The present paper examines whether supplier inducement exists for primary physicians' services in Norway. Our model assumes optimization behavior of the physician. The research design is adapted to the institutional setting of Norwegian primary physician services, where there is a fixed fee schedule. According to our model, the physician has three choices: to rational services, to supply an optimal amount of services, or to induce demand for services. The analyses revealed no indication of inducement with respect to physician-initiated visits. However, supplier inducement effects were found for provision of laboratory tests.

Contract Services↗
PubMed1994

Hospital financing in Norway.

The Norwegian block grant reform of 1980 replaced state reimbursements to hospitals by block grants allocated to counties according to objective criteria. The reform was accompanied by a general decentralization of budget authority to local level. The reform aimed to promote primary care, equalize the supply of health care across regions and give counties incentives to improve hospital efficiency. A decade later, the reform was reversed. The government has imposed restrictions which reduce the budget discretion of the counties and part of the block grant has been made dependent on the performance of the hospitals in the counties. The government has also issued a 'waiting-list guarantee' which states that patients who suffer from a serious disease are entitled to medical treatment within six months. This paper provides an overview of hospital financing in Norway during the last two decades and discusses why the block grant system did not fulfil the expectations of its architects.

Budgets↗
PubMed1987

Schmidt-Lanterman clefts: a morphometric study in human sural nerve.

In the human sural nerve, large myelinated fibers contained 35 Schmidt-Lanterman (SL) clefts per mm, and small myelinated fibers contained only eight SL clefts per mm. The incidence of SL clefts is linearly related to myelin thickness. The SL clefts extended over 13 micron in large and over 9 micron in small fibers, the total extent of the SL region amounting to nearly 50% of internodal length in large and to 6% in small fibers. In the SL region, the fiber diameter was 6% larger than outside this region, and the axon was 17% smaller in large and 28% smaller in small fibers. The paranodal-nodal region occupied less than 2% of internodal length in large fibers and 6.5% in small fibers; in the nodal region the axon diameter was reduced by 40-50%.

Adult↗
PubMed1980

Three dimensional analysis of Schwann cells associated with unmyelinated nerve fibres in human sural nerve.

In a cross section the profile of one or several unmyelinated axons is embraced by profiles of one or several Schwann cells, all surrounded by a basal lamina. Reconstructions demonstrate that this complex structure is the result of overlap and regrouping of contiguous Schwann cells and only to a lesser extent to branching of Schwann cells. More than half the 36 Schwann cells reconstructed did not branch within the 200 micrometer analysed, and one fourth had two branches. Notwithstanding the regrouping of Schwann cells and axons at different levels of the nerve, the number of Schwann cell subunits in a single cross section is a suitable gauge for the number of Schwann cells. The single nucleus is situated midway between the ends of the Schwann cell. The length of the Schwann cells ranges from 220 to somewhat more than 400 micrometer; the thickness is 0x2-0x5 and in the region 2-5 micrometer. Collagen pockets are outpouchings of the Schwann cell which rarely extend over more than 6 micrometer along the Schwann cell; they are spaced at average intervals of 20 micrometer. Outpounchings devoid of collagen pockets have a similar length but occur more rarely. Abnormally dense cytoplasm, when present, is seen throughout the entire length of the Schwann cell.

Adult↗
PubMed1977

Apatite crystals in pseudoxanthoma elasticum: a combined study using electron microscopy and selected area diffraction analysis.

Calcium deposits in elastic fibers of involved skin of patients suffering from pseudoxanthoma elasticum have previously been reported. In the present work, the crystalline structure and composition were studied. Involved skin was obtained from 5 patients. Bright-field and dark-field electron microscopy and selected area electron diffraction of the calcium deposits were applied. The study demonstrates calcium apatite crystals.

Apatites↗
PubMed1977

Nerve biopsy and conduction studies in diabetic neuropathy.

Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.

Adult↗
PubMed1975

Unmyelinated fibres and Schwann cells of sural nerve in neuropathy.

Electron micrographs of 45 sural nerves from patients with acquired (22) or heredodegenerative neuropathy (23) were analysed with respect to the number of unmyelinated nerve fibres, 37 nerves with respect to the number of Schwann cell sub-units and of structures connected with Schwann cells. Findings were compared with those in 6 nerves from control subjects and referred to the total number rather than to the number per mm2 to eliminate error due to increase in the transverse endoneurial area, present in more than half the diseased nerves. Ninety-one per cent of the diseased nerves showed one or several abnormalities in unmyelinated fibres of their Schwann cells. The best indicator of fibre loss was an increase in the number of Schwann cell sub-units devoid of axons, found in more than half the nerves. This was the only abnormality related with decrease in number of myelinated fibres. The increase in number of empty Schwann cell sub-units was due both to loss of unmyelinated nerve fibres and to proliferation of Schwann cells. Proliferation was indicated by the higher incidence of Schwann cell nuclei in cross-sections of diseased nerves than in controls. The earliest sign of involvement was an increase in number of profiles and of small isolated Schwann cell projections, observed in 33 of 37 diseased nerves, as the only abnormality in 7 nerves. The number of unmyelinated nerve fibres by itself was of little value to indicate loss of fibres, since regeneration often replaced or more than replaced degenerated fibres. Regeneration was indicated by an increase in number or incidence of small unmyelinated fibres, present in nearly half of 45 diseased nerves; and by an increased in the total number, present in a third of the nerves. An increase in the number of collagen pockets and of fibres undergoing degeneration (loss of organelles) and a decrease in the number of unmyelinated fibres per Schwann cell sub-units was present in only a quarter to a third of diseased nerves and was not related to other criteria of loss of fibres or of regneration.

Adolescent↗
PubMed1968

The ultrastructure of the M line in skeletal muscle.

By electron microscopy, the ultrastructure of the M line was investigated in fibers from frog nonglycerinated semitendinosus muscles at body length and at different degrees of shortening and stretch. The M line appeared as a line of high electron opacity in the middle of the A band. Its framework consists of: (i) three (four or five) arrays of transverse M bridges, 200 A apart, connecting each A filament with its six neighbors; (ii) M filaments, parallel to the A filaments, passing through the M line and linking each set of M bridges together. In the shortened fiber the M line remained distinct. At high degrees of stretch, the M line became fainter or indiscernible. This appearance reflects a misalignment of the M components caused by a staggering of the A filaments. The M line reappeared after release of fibers stretched 70-80% above equilibrium length. On the basis of the structural analysis, the possible function of the M line is compared with that of the Z line, and a model is suggested for the M line.

Animals↗
PubMed1965

Contractility and ultrastructure in glycerol--extracted muscle fibers. I. The relationship of contractility to sarcomere length.

This study was undertaken to determine whether glycerol-extracted rabbit psoas muscle fibers can develop tension and shorten after being stretched to such a length that the primary and secondary filaments no longer overlap. A method was devised to measure the initial sarcomere length and the ATP-induced isotonic shortening in prestretched isolated fibers subjected to a small preload (0.02 to 0.15 P(0)). At all degrees of stretch, the fiber was able to shorten (60 to 75 per cent): to a sarcomere length of 0.7 micro when the initial length was 3.7 micro or less, and to an increasing length of 0.9 to 1.8 micro with increasing initial sarcomere length (3.8 to 4.4 micro). At sarcomere lengths of 3.8 to 4.5 micro, overlap of filaments was lost, as verified by electron microscopy. The variation in sarcomere length within individual fibers has been assessed by both light and electron microscopic measurements. In fibers up to 10 mm in length the stretch was evenly distributed along the fiber, and with sarcomere spacings greater than 4 micro there was only a slight chance of finding sarcomeres with filament overlap. These observations are in apparent contradiction to the assumption that an overlap of A and I filaments is necessary for tension generation and shortening.

Adenosine Triphosphate↗
PubMed1965

Contractility and ultrastructure in glycerol--extracted muscle fibers. II. Ultrastructure in resting and shortened fibers.

Glycerol-extracted rabbit psoas muscle fibers were examined by electron microscopy both before and after ATP-induced isotonic shortening. Ultrastructural changes were correlated with the initial sarcomere length and the degree of shortening. The ultrastructural appearance of the resting fiber at rest length was identical with that described by H. E. Huxley and Hanson. At sarcomere lengths greater than 3.7 to 3.8 micro, the A and I filaments were detached and separated by a gap. The presence of "gap" filaments was confirmed, and evidence is presented which indicates that these filaments form connections between the ends of the A and I filaments. Shortening from initial sarcomere lengths at which the filaments overlapped took place through sliding of the filaments. If shortening was initiated from sarcomere lengths at which there was a gap, a narrowing of the I band was brought about by a curling of the I filaments at the boundary between the A and I bands. No evidence could be found that the I filaments moved into the A band.

Animals↗
PubMedDate not supplied

Histology and ultrastructure of alterations in neuropathy.

Histologic findings are described in nerves from men exposed to lead, from patients with discrete clinical signs of peripheral neuropathy, and from controls. Every nerve from control subjects showed an abnormality (paranodal remyelination, segmental remyelination, or regeneration) in teased fibers. The only histologic alteration in eight lead-exposed males without signs or symptoms of neuropathy was a slightly increased incidence of paranodal remyelination. Sixteen patients with discrete neurologic symptoms and signs had a loss of large myelinated fibers and an increased incidence of regenerated fibers among teased fibers. Electron microscopy of unmyelinated fibers showed an increased occurrence of Schwann-cell processes, of fibers undergoing degeneration, and of Schwann-cell subunits with many profiles as the earliest signs of abnormality. Clinically mild neuropathies may exhibit advanced regeneration in the case of unmyelinated fibers. The earliest sign of degeneration in myelinated fibers was a diminution in the number of axonal organelles.

Adult↗