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Biomedical subjects

B Møller-Madsen

Publications and source records attributed to B Møller-Madsen.

At least 19 recordsLinked to original sources
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↗
PubMed1991

Localization of mercury in CNS of the rat. III. Oral administration of methylmercuric chloride (CH3HgCl).

The distribution and cellular localization of mercury in the in situ brain and upper cervical spinal cord of adult Wistar rats were studied at various time intervals after oral administration of methylmercuric chloride (CH3HgCl; 20 mg x liter-1). Coronal sections of the brain and transverse sections of the cervical spinal cord were prepared for visualization of the mercury by the autometallographic silver-enhancement method. Following mercury administration there was a latent period before the metal appeared in the tissue. Mercury staining was first detected after 10 days in cell bodies of five specific areas of the brain stem: the mesencephalic nucleus of the trigeminal nerve, the red nuclei, the ventral cochlear nucleus, the superior vestibular nucleus, and the nucleus reticularis pontis caudalis. After 28 days of treatment, a fairly even distribution of mercury was seen in the brain and spinal cord. Longer periods of treatment caused no further increase in the density of mercury within the stained cell bodies. In cerebral cortex, staining commenced in piriform and entorhinal cortices. This was followed by staining in neurons of lamina III in the isocortex and ultimately all layers were stained after 28 days of treatment. After 20 days of treatment, mercury deposits in the cerebellar cortex were restricted to Purkinje cells, Golgi epithelial cells, and Golgi cells, while in the spinal cord the majority of mercury was located in the anterior horn motoneurons. Scattered ependymal cells and epithelial cells of the choroid plexus also exhibited mercury staining. The principal target cells were neurons followed by the glial and ependymal cells. Ultrastructurally, the bulk of detectable mercury was localized in lysosomes.

Animals↗
PubMed1990

Autometallographic demonstration of gold in the adrenal gland of rats exposed to sodium aurothiomalate. A light and electron microscopic study.

The presence of gold was investigated in sections of the adrenal glands from rats which had been exposed to intraperitoneal sodium aurothiomalate (32 to 120 mg). Gold was histochemically detected in cortical endocrine cells, chromaffin cells and in fibroblasts and macrophages of both the cortex and medulla. Invisible traces of gold were silver enhanced by autometallography making them readily visible at both the light and electron microscopic levels. The intracellular staining intensity was dose-dependent. In general, the number as well as the staining intensity of individual cells, were highest in the zona glomerulosa and zona reticularis. In gold-containing cells the silver-amplified deposits were present in lysosomes.

Adrenal Glands↗
PubMed1990

Missed injuries in an orthopaedic department.

In a prospective study lasting 6 months, all missed injuries in patients visiting the casualty department or admitted to the orthopaedic department of Aarhus Amtssygehus were registered and analysed. A total of 15,806 patients attended the casualty department and 783 patients were admitted to the orthopaedic department. Eighty-four injuries were missed in 83 patients in the casualty department, making a missed injury rate of 0.5 per cent. Twenty-three injuries were missed in 17 patients in the orthopaedic department making a missed injury rate of 2.2 per cent. Re-examination of all patients and matching radiographs reduced the number of missed injuries significantly.

Adolescent↗
PubMed1990

Localization of mercury in CNS of the rat. II. Intraperitoneal injection of methylmercuric chloride (CH3HgCl) and mercuric chloride (HgCl2).

The autometallographic method has been used to determine the precise localization of mercury in the brain and spinal cord of adult Wistar rats which had been treated with repeated ip injections of methylmercuric chloride (CH3HgCl; 0.2 to 10.0 mg) or mercuric chloride (HgCl2; 0.2 to 10.0 mg). The distribution of mercury was uneven following administration of HgCl2, while it was fairly homogeneous following CH3HgCl. With both compounds, however, heavy deposits of mercury were present in the motor nuclei of rhombencephalon. In contrast, cerebellar Purkinje cells, Golgi cells, and Golgi epithelial cells only contained mercury in sections from rats exposed to CH3HgCl. In cerebral sections from rats exposed to CH3HgCl, staining intensity in cortical cells varied among the layers, being greatest in laminae III, V, and VI. On the other hand, sections from rats exposed to HgCl2 showed only staining in scattered cells of lamina VI. Following administration of either compound, mercury was detected in the gray matter of the spinal cord mercury. Particularly large deposits were present in the anterior horn motoneurons. At the cellular level, the heaviest staining intensity was seen in neurons, although the cytoplasm of glia and ependymal cells also showed significant deposits in sections from rats exposed to CH3HgCl. In HgCl2-treated rats, the largest accumulations of mercury were seen in the neurons. The ependymal cells were stained to a lesser extent, while glia were devoid of mercury. Ultrastructurally, mercury deposits were located exclusively in lysosomes. The present results demonstrate that the pattern of mercury distribution and its staining intensity in individual cells in the rat CNS are dependent upon the chemical structure of the compound and the duration of its administration.

Animals↗
PubMed1990

Amalgam associated mercury accumulations in normal oral mucosa, oral mucosal lesions of lichen planus and contact lesions associated with amalgam.

Fourty-three patients with oral mucosal lesions were divided into 3 groups based on the relationship between lesions and amalgam restorations. Group I consisted of patients with contact lesions confined to mucosal areas in contact with amalgam fillings. Group II patients had lichen planus lesions exceeding the area of contact with an amalgam filling and Group III comprised patients with lichen planus lesions without relation to amalgam fillings. Biopsies were embedded in epon and subjected to autometallography in order to demonstrate a possible accumulation of mercury in the affected mucosa. In 20 our of 21 patients in Group I, 4 of 11 patients in Group II and 4 of 11 patients in Group III, mercury was found in the lysosomes of macrophages and fibroblasts. In Group I the number of cells loaded with mercury was much higher than in Group II and in particular Group III. In the latter groups autometallographically demonstrated mercury was found almost exclusively in macrophages. Nineteen biopsies taken from patients with normal mucosa served as controls. Ten had occlusal (Group IV) and seven buccal fillings (Group V). The biopsies from the latter group were taken from areas opposing amalgam restorations. Two patients had no amalgam fillings (Group VI). The histochemical technique showed that three biopsies in Group IV (occlusal fillings only) and two in Group V (opposing buccal fillings) contained traces of mercury in the juxtaepithelial connective tissue. The silver enhanced mercury was found in macrophages. The two controls (Group VI) without amalgam fillings were devoid of precipitates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Skiing injuries: a study from a Danish community.

A Danish investigation of skiing injuries is presented from the casualty wards of two hospitals. The material consisted of 119 skiing injuries. Fifty-three per cent of the patients were women. Eighty-three injuries occurred abroad, mainly in Austria and Norway. Injury rate was not related to sex. The highest injury rate was found in the age group 20 to 29 years old. The most frequent injuries were sprains (knee 43, finger 14), fractures (39) and contusions (19). Injuries requiring hospitalization were common. None of these resulted in permanent major disability.

Adult↗
PubMed1990

Badminton injuries.

In a one year period, from 1 January 1986 to 31 December 1986, 4303 patients with sports injuries were treated at Aarhus Amtssygehus and Aarhus Kommunehospital. The mean age was 21.6 years (range 7-72 years) and 2830 were men. Two hundred and seventeen badminton injuries occurred in 208 patients (136 men) with a mean age of 29.6 years (range 7-57 years), constituting 4.1 percent of all sport injuries in Aarhus. Joints and ligaments were injured in 58.5 percent of the patients, most frequently located in the lower limb and significantly more often among patients younger than 30 years of age. Muscle injury occurred in 19.8 percent of the patients. This type of injury was significantly more frequent among patients older than 30 years of age. Most injuries were minor. However, 6.8 percent of the patients were hospitalized and 30.9 percent received additional treatment by a physician. As the risk of injury varies with age, attempts to plan training individually and to institute prophylactic measures should be made.

Adolescent↗
PubMed1989

Silver enhancement of tissue mercury: demonstration of mercury in autometallographic silver grains from rat kidneys.

The autometallographic silver enhancement method has been applied increasingly to detect trace amounts of mercury in preparations of biological tissue. It has, however, been difficult to establish the presence of a core of mercury within the silver grain by direct methods such as energy dispersive X-ray analysis. In the present work, a sample of autometallographic silver grains was prepared from kidneys of rats exposed to mercury in the drinking water. Frozen sections from the kidneys were silver-enhanced and subsequently all organic material was removed by enzymatic digestion. The remaining pellet of silver grains was analyzed by proton-induced X-ray emission (PIXE) and mercury was demonstrated in an amount of 0.1-0.5% compared to silver. In addition, it was demonstrated that two pools of catalytic mercury compounds exist, probably corresponding to sulfide- and selenium-bound mercury.

Animals↗