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B Møller-Madsen

Publications and source records attributed to B Møller-Madsen.

At least 19 recordsLinked to original sources
PubMed2004

Autometallographic tracing of zinc ions in growing bone.

It has previously been established that zinc (Zn) supplementation increases bone dimensions and strength in growing rats. The present study aims at describing differences in the localization of loosely bound or free zinc ions, as revealed by autometallography (AMG), that might take place in the skeleton of growing rats following alimentary zinc depletion and supplementation. Male Wistar rats, 4 weeks old, were randomly divided into three groups. The rats had free access to a semi-synthetic diet with different amounts of zinc added. Group 1 was given a zinc-free (2 mg zinc/kg) diet, group 2 a 47 mg zinc/kg diet, and group 3 a 60 mg zinc/kg diet. All animals were killed after 4 weeks. Animals from each group were transcardially perfused with a 0.1 % sodium sulphide solution according to the zinc specific Neo-Timm method causing zinc ions to be bound in AMG catalytic zinc-sulphur clusters. We found clusters of zinc ions localized in the mineralizing osteoid in all groups. No immediate differences in AMG staining intensity could be observed between the groups neither in the uncalcified bone nor in the osteoblasts. However, alimentary zinc supply resulted in an increase in the height of the total growth plate in a dose-dependent manner. Zinc ions were also observed in chondrocytes throughout the whole thickness of the articular and the epiphyseal cartilage as well as in the inner layer of the synovial membrane.

Animals↗
PubMed2001

[Osteogenesis imperfecta. The effect of intramedullary nails in long tubular bones].

INTRODUCTION: The aim of the study was to describe the clinical, radiological, and functional results of intramedullary nailing of deformities in the lower extremities of children with osteogenesis imperfecta after the use of multiple osteotomies and non-telescoping rods (rush pins). MATERIAL AND METHODS: Eight children with osteogenesis imperfecta, who consecutively underwent surgery during 1991-1994, were entered in the study. RESULTS: Sixteen operations were performed on eight children: 12 on the femur and four on the tibia. Like others, we found a high complication rate, 50%. Radiological correction of angular deformities was good. The functional outcome was satisfactory and the patients were satisfied. CONCLUSION: Correction and stabilisation of deformities in the lower extremities in children with osteogenesis imperfecta with the use of non-telescoping rods is an acceptable method of decreasing fractures and allowing most formerly non-ambulatory children to walk. Furthermore, the cosmetics were improved.

Adolescent↗
PubMed2001

The positive effects of zinc on skeletal strength in growing rats.

The aim of the present study was to assess the skeletal effects of alimentary zinc depletion and supplementation in an animal model of intact, growing rats. The study was planned as a dose-response study. Thirty-six male Wistar rats, 4 weeks old, were divided into three groups of 12 rats each. The rats had free access to a semisynthetic diet with different amounts of zinc added. Group 1 was given a zinc-free diet containing 2 mg zinc/kg, group 2 was given a normal-zinc diet containing 47 mg zinc/kg; and group 3 was given a zinc-supplemented diet containing 60 mg zinc/kg. All animals were killed 4 weeks after initiation of the experiment and the right femora were removed. The biomechanical effects were measured at the following skeletal sites: femoral diaphysis; femoral neck; and distal femoral metaphysis. In addition, static histomorphometry was performed at the middiaphyseal region. Biomechanical testing revealed a significant zinc-induced increase in bone strength at all sites investigated. It also showed that zinc influenced bone strength in a dose-dependent manner except at the distal metaphysis, where there was no significant difference between the group fed normal-zinc diet and the group fed a hyper-zinc diet. Zinc also improved the rates of growth in the rats. The body weights and length of femora increased dose-dependently. Static histomorphometry showed that zinc exerted its main effect on the periosteal envelope, thereby increasing bone area, tissue area, and axial moment of inertia. We conclude that alimentary zinc supplementation in growing rats induces an increase of bone strength in both the femoral neck and the femoral diaphysis. These results further support the view that zinc has a positive effect on bone metabolism which mimics that of growth hormone (GH) or insulin-like growth factor 1 (IGF-1).

Animals↗
PubMed1997

The effect of selenium on the localization of autometallographic mercury in dorsal root ganglia of rats.

The autometallographic technique was used to demonstrate the localization of mercury in dorsal root ganglia of adult Wistar rats. The animals were either exposed to mercury vapour, 100 micrograms Hg m-3, 6 h day-1, 5 days per week, or treated with organic mercury in the drinking water, 20 mg CH3HgCl per litre, for 4 weeks. The effect of orally administered sodium selenite on the pattern of intracellular distribution of mercury in these two situations was investigated. In rats exposed to mercury vapour alone, faint staining was present in ganglion cells. The selenite induced a conspicuous increase in the number of stained cells and in the intracellular staining intensity. In rats treated with organic mercury, mercury deposits were detected within ganglion cells and macrophages. The number of mercury-containing cells was increased by co-administration of selenite. In addition, satellite cells, the capsule and vessel walls were faintly stained. Twenty weeks after cessation of the organic mercury treatment, mercury staining was reduced. Again, selenite treatment enhanced staining intensity. When studied using the electron microscope, mercury was restricted to lysosomes, irrespective of treatments. The present study shows that the deposition of autometallographic mercury in the dorsal root ganglia depends on the chemical type of mercury, the co-administration of selenite and the length of the survival period.

Administration, Inhalation↗
PubMed1995

Volleyball injuries presenting in casualty: a prospective study.

During 1986, all sports injuries (n = 5222) were prospectively recorded at the two casualty departments in Arhus, Denmark. Volleyball injuries (n = 278) accounted for 5.3% of all sports injuries. An evaluation of the rehabilitation period and the consequences of the injuries was undertaken by questionnaire three years after the injury. The injury incidence was 1.9 injuries/1000 inhabitants/year. Hand, finger, and ankle sprains were the most frequent injuries. Female players had significantly more hand/finger injuries than male players, who incurred more ankle/foot injuries. Knee (6%) and ankle injuries (31%) were responsible for the longest duration of absence from sports participation. There were relatively few chronic injuries. The study suggests the need to enhance prophylactic measures with regard to blocking and overhand pass techniques, in order to reduce the number and extent of ankle and hand/finger injuries.

Adolescent↗
PubMed1993

Detection of mercury in rat spinal cord and dorsal root ganglia after exposure to mercury vapor.

Adult male Wistar rats were exposed to mercury vapor, 50 micrograms Hg/m3, 6 hr/day, 5 days/week, over 1-, 2-, 3-, 4-, 6-, and 8-week periods. Sections from the spinal cord and dorsal root ganglia from spinal levels C1, C5, T6, and L1 were stained with the autometallographical technique and the distribution of mercury deposits described at light and electron microscopical levels. A quantitative analysis of the amount of mercury in blocks of the spinal cord was performed using cold vapor atomic absorption spectrophotometry. After an exposure period of 2 weeks, silver-enhanced mercury grains could be observed in spinal cord neurons located in Rexed laminae IV-X. Ventral horn motoneurons were heavily stained in all of the spinal cord segments. Ependymal cells and glial cells of both the spinal gray and white matter contained cytoplasmatic mercury accumulations in rats exposed to mercury vapor for 4 weeks. In the dorsal root ganglia, only ganglion cells showed a faint mercury staining and the amount of staining was notably less than that seen in the ventral horn motoneurons. At the ultrastructural level, mercury was seen primarily within lysosomes of target cells. The quantitative mercury measurements demonstrated that spinal cords from rats exposed to mercury vapor for 6 or 8 weeks contained a significantly higher concentration of mercury than those from control animals.

Administration, Inhalation↗
PubMed1993

Differentiation of silver-enhanced mercury and gold in tissue sections of rat dorsal root ganglia.

Autometallography was used in conjunction with light and electron microscopy to detect traces of gold and mercury in the dorsal root ganglia of rats treated with sodium aurothiomalate and mercuric chloride. In order to differentiate between gold and mercury in tissue sections, the gold accumulations were removed by potassium cyanide, leaving mercury sulphides/selenides as the only possible catalysts for autometallographic development. With this technique, it is now possible to differentiate between all tissue metals capable of initiating the autometallographic process, i.e. gold, vesicular zinc, and sulphides and selenides of mercury and silver.

Animals↗
PubMed1992

Localization of mercury in CNS of the rat. V. Inhalation exposure to metallic mercury.

The autometallographical technique has been used to determine the distribution and cellular localization of mercury deposits in the Wistar rat CNS after exposure to elemental mercury vapor (50-550 micrograms Hg/m3 of air for 4-24 h). In animals exposed to 50 micrograms Hg/m3 for 8 h, silver-enhanced mercury grains were confined to the capillary walls. Increasing the concentration of mercury to 500 micrograms Hg/m3 caused mercury staining to appear in neurons in the corpus striatum, mesencephalic nucleus of the trigeminal nerve and cerebellar deep nuclei. In the spinal cord, mercury appeared primarily in the motoneurons of lamina IX. Following exposure to 550 micrograms Hg/m3 for 12 h mercury was additionally detected in the ependyma. Animal exposure to 550 micrograms Hg/m3 for 24 h resulted in visible mercury deposits in the cerebellar and cerebral cortices. In the cerebral cortex, mercury was present in neurons populating lamina III in the isocortex. No mercury was detected in the allocortex. In the cerebellar cortex, mercury staining was limited to the Purkinje cells. Neurons in the thalamus contained heavy accumulations of mercury. Heavy staining for mercury was detected in lung alveolar macrophages in sections prepared from animals exposed to 550 micrograms Hg/m3 for 24 h. In animals exposed to 500 micrograms Hg/m3 or more, the primary target cells were the neurons, but glia cells also contained scattered mercury deposits. Ultrastructurally, mercury deposits were detected in the lysosomes.

Administration, Inhalation↗
PubMed1992

Autometallographic detection of mercury in rat spinal cord after treatment with organic mercury.

Autometallography was used to localize mercury in rat spinal cord after intraperitoneal administration of methylmercuric chloride (200 micrograms CH3HgCl daily). The technique permits small amounts of mercury sulfides and mercury selenides to be visualized by silver-enhancement. Mercury deposits were observed by light microscopy only in neurons. In all of the spinal cord segments selected (first cervical segment, C1; fifth cervical segment, C5; sixth thoracic segment, T6; and first lumbar segment, L1) the mercury was observed with cumulative dosages of 6000 micrograms CH3HgCl and greater. Laminae VII, VIII, and IX contained the majority of stained neurons, whereas laminae IV, V, VI, and X had a relatively lower density of mercury-containing neurons. Stained neurons were confined to specific cell groups, such as Clarke's column, nucleus intermedio-lateralis, nucleus cervicalis centralis, and nucleus dorsomedialis. At the ultrastructural level, mercury deposits were restricted to lysosomes of neurons and occasional accumulations in the lysosomes of ependymal cells.

Animals↗
PubMed1992

Autometallographic detection of gold in dorsal root ganglia of rats treated with sodium aurothiomalate.

Ultraviolet light autometallography, a very sensitive method for gold detection, was applied to sections of dorsal root ganglia from adult male Wistar rats treated with intraperitoneal injections of sodium aurothiomalate. Silver-amplified traces of gold were detected within the cytoplasm of ganglion cells, satellite cells, Schwann cells, macrophages, endothelial cells, and fibroblasts throughout the ganglia. Gold was never detected in axons nor myelin sheaths. In the electron microscope, gold deposits were restricted to the lysosomes irrespective of cell type or dosage.

Animals↗
PubMed1991

Autometallographic mapping of mercury deposits in the spinal cord of rats treated with inorganic mercury.

The autometallographic method has been used in conjunction light and electron microscopy to determine the exact localization of mercury in the rat spinal cord. Adult male Wistar rats were treated intraperitoneally with accumulative doses of mercuric chloride (100-200 micrograms HgCl2 daily). Transverse sections of the first cervical segment (C1), fifth cervical segment (C5), sixth thoracic segment (T6), and first lumbar segment (L1) of the spinal cord were examined. The distribution pattern of mercury was dose dependent. In ventral horn motoneurons and neurons of nucleus dorso-medialis (C1) pronounced staining was found after a total dosage of 1200 micrograms HgCl2. In nucleus intermedio-lateralis (T6, L1) and nucleus cervicalis centralis (C1) stained neurons were first seen after 2600 micrograms HgCl2. Ultrastructurally, mercury deposits were exclusively located in lysosomes of neurons, astrocytes, endothelial cells, and ependymal cells.

Animals↗
PubMed1991

Localization of mercury in CNS of the rat. IV. The effect of selenium on orally administered organic and inorganic mercury.

The distribution and exact cellular localization of mercury in the brain and upper cervical spinal cord of the adult male Wistar rat has been determined using the autometallographic silver-enhancement technique. A detailed atlas of mercury-containing nuclei following oral administration of HgCl2 (20 mg x liter-1 or CH3HgCl (20 mg x liter-1) was prepared. The effect of orally administered Na2SeO3 (2 mg x liter-1) on these patterns was investigated. In animals treated with CH3HgCl, sodium selenite induced a conspicuous increase in mercury staining of nerve cell bodies in specific areas of the central nervous system (CNS) including laminae III-VI in the cerebral cortex, thalamus, hypothalamus, and brain stem nuclei. In the cerebellum, the cortical Purkinje cells and nerve cells in the deep nuclei were targets for appreciable mercury accumulations after CH3HgCl. Again, these deposits were increased by coadministration of selenite. In the spinal cord following administration of CH3HgCl alone, staining was limited to the gray matter. The intensity of this staining was increased by selenite and deposits also appeared in the white matter. Mercury accumulations were present in scattered glia cells in the cuneate and gracile fasciculi. Treatment with HgCl2 alone or in combination with selenite yielded no staining of the Purkinje cells, nor did selenite result in an increase in the density of other stained cell bodies throughout the CNS, as was the case with organic mercury. The most intense neuronal staining was seen in sections taken from rats treated with a combination of CH3HgCl and selenite. Lesser staining was seen in neuroglia, ependymal, and choroidal cells. In the latter two cell types, staining intensity was unaffected by selenite treatment. In HgCl2-treated rats the same cell types were targets for mercury deposits although staining was to a significantly lesser degree. Concurrent treatment with selenite had no visible effect on the staining pattern. Ultrastructurally, the bulk of the mercury was located in lysosomes. Administration of CH3HgCl combined with selenite caused mercury to appear in the nuclei of neurons. Selenium treatment delayed the functional toxic effects of CH3HgCl. Sections prepared from animals treated separately with selenium or demineralized water (used as the solvent for all compounds) were devoid of mercury deposits.

Animals↗
PubMed1991

Ultrastructural demonstration of mercury in Sertoli and Leydig cells of the rat following methyl mercuric chloride or mercuric chloride treatment.

The autometallographic silver enhancement technique has been used to demonstrate the ultrastructural localization of mercury in the testes of adult rats. Administration of mercuric chloride or methyl mercuric chloride in the drinking water (20 mg/L for 12 weeks) resulted in intracellular accumulations of mercury in the interstitial Leydig cells as well as in the Sertoli cells of the seminiferous tubules.

Animals↗
PubMed1991

Mercury in the dorsal root ganglia of rats treated with inorganic or organic mercury.

Autometallographic silver amplification has been used to demonstrate the localization of mercury deposits in rat dorsal root ganglia after repeated intraperitoneal injections of mercuric chloride or methylmercuric chloride. The silver-enhanced mercury deposits were demonstrated with the light and electron microscope. The degree of intracellular staining of the individual cells depended on the mercury compound and total dosage. Ganglion cells (types A and B) and macrophages were found to accumulate mercury after a total dosage of 400 micrograms HgCl2. After 600 micrograms HgCl2, satellite cells, endothelial cells and fibroblasts were additionally found to contain mercury deposits. Treatment with 6000 micrograms CH3HgCl caused faint staining of type A and B ganglion cells and fibroblasts. Macrophages, however, were the most heavily stained cells after treatment with CH3HgCl. Ultrastructurally, mercury was exclusively located in lysosomes. This was irrespective of the cell type and mercury compound used for treatment.

Animals↗