Biomedical subjects

T Bredehorn

Publications and source records attributed to T Bredehorn.

28 records · Page 2Linked to original sources

PubMed2001

[Incidence of potential transmitters of Creutzfeldt-Jakob disease. A study of a collective of potential cornea donors].

BACKGROUND: The prevalence of Creutzfeldt-Jakob disease (CJD) is 1.5 cases per million persons. In addition to familial and sporadic forms, fewer than 5% of cases are due to iatrogenic transmission. Corneal transplantation has clearly been implicated as the origin of CJD in four cases. MATERIALS AND METHODS: We examined possible risks factors for corneal transplantation in material from 2545 deceased patients at the University Hospital of Halle. RESULTS: Two patients had died of CJD or slow virus disease. Also in the 109 identified as being at higher risk of CJD no organs or tissues were harvested. CONCLUSION: We strongly recommend that patients at higher risk group of CJD, patients dying of CNS diseases of unknown origin and cause, and patients dying in psychiatric clinics be excluded from donating organ and tissue.

Adult↗

PubMed2001

Morphological and functional changes due to drug-induced lysosomal storage of sulphated glycosaminoglycans in the rat retina.

UNLABELLED: A series of dicationic amphiphilic drugs, most of them immunomodulatory agents, are known to induce generalised lysosomal storage of sulphated glycosaminoglycans (GAGs) in rats and in cultured cells of several species including man. The present study deals with the cytological effects of two experimental immunomodulatory acridine derivatives upon the retina of rats. The animals were treated orally with compound CL-90.100 (3,6-bis[2-(diethylamino)ethoxy]acridine) or an analogue for periods up to 22 weeks at a dose range of 60-90 mg/kg body weight and the retinae examined by light and electron microcopy. ERG measurements were done initially and after 16 weeks of treatment. All types of retinal cells developed abnormal cytoplasmic vacuoles which represented the ultrastructural counterpart of lysosomal GAG storage as demonstrated by histochemical and cytochemical staining experiments. The retinal pigment epithelium and the Müller cells were most prominently affected, photoreceptor cells to a lesser degree, and retinal neurons to varying degrees. The topographical distribution of the drug as detected by fluorescence microscopy closely resembled the distribution of the GAG accumulation in the retinal layers. After treatment for 16 weeks, the a-and b-wave amplitudes in the ERG were significantly reduced compared with the controls. CONCLUSION: the glycosaminoglycan storage in pigment epithelium is reminiscent of that seen in some inherited mucopolysaccharidoses of humans. When a given cell type shows lysosomal accumulation of glycosaminoglycans as a consequence of impaired degradation, it can be assumed to be engaged in the turnover of glycosaminoglycans under normal conditions. Thus the present results suggest that not only the retinal pigment epithelium but also Müller cells, photoreceptor cells, and, to variable degree, retinal neurons are normally involved in the catabolism of sulphated glycosaminoglycans. We believe that the lysosomal storage of glycosaminoglycans caused secondary cellular disturbance responsible for the functional changes shown by electroretinography.

Acridines↗

PubMed2001

[Investigations on the cornea donation at the Martin-Luther-University Halle-Wittenberg].

AIM: We analysed the number of the potential cornea donors of the Martin-Luther-University, Halle-Wittenberg over a four-years period, 1995 to 1998 in relationships to the number of the actual donors. PATIENTS AND METHODS: We retrospectively reviewed the data of 2545 patients who died at the hospitals of the Martin-Luther-University, Halle-Wittenberg over a four-years period, from January 1995 to December 1998. The medical records of the patients were inspected and contraindications for cornea donation examined. The patients who were younger than 12 months were omitted in our analysis. The patients with at least one contraindication were excluded as potential cornea donors. Additionally we registered the actual cornea donors of the hospitals of the Martin-Luther-University, Halle-Wittenberg between 1995 to 1998. RESULTS: The mean age of the died patients was 60 years. Because of contraindications 597 patients (23.5 %) were excluded from the cornea donation. An acute sepsis with 25.1 % as well as leukemias and lymphomas with 24.8 % matched about half of the exclusion criteria. In the period of investigation we counted 1948 potential cornea donors. In the hospitals of the Martin-Luther-University, Halle-Wittenberg only 57 (2.9 % of potential donors) actual cornea donors have been registered. CONCLUSIONS: The possible leading causes for the large discrepancy between the number of the potential and actual donors are: (1) the imperfect identification of potential donors, (2) the donor family have not been asked and (3) the denial of consent by the potential donors family.

Adolescent↗

PubMed2000

[Tilorone-induced functional changes in the rat retina].

BACKGROUND: The amphiphilic interferon-inducing drug tilorone belongs to the group of synthetic fluorenone with antitumorus and antiviral effects and is known to cause lipidosis in the human and rat retina. METHODS: We treated female albino Wistar-Kyoto-Rats and Spontaneously-Hypertensive-Rats orally with tilorone for 8 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. RESULTS: Tilorone caused moderate lipidosis in the ganglion cells and slight lipidosis in the pigment epithelium after 8 weeks of treatment with a stronger effect in Spontaneously-Hypertensive-Rats. The b-wave amplitude was reduced by 30% compared to controls in Spontaneously-Hypertensive-Rats and by 10% in the Wistar-Kyoto-group. The a-wave amplitude was reduced by 25% in Spontaneously-Hypertensive-Rats. CONCLUSION: Tilorone induced lipidosis shows a clear affinity to ganglion cells. The electroretinographic changes in Spontaneously-Hypertensive-Rats are most likely caused by the severe lipidosis in the neuroretina compared to the Wistar-Kyoto-group.

Animals↗

PubMed1999

[Chloroquine- and chlorphentermin-induced lipidosis in rat retina].

BACKGROUND: The amphiphilic drugs chloroquine and chlorphentermine are known to cause lipidosis in the human and rat retina. METHODS: We treated femal albino Wistar rats orally with chloroquine for 12 weeks, followed by a period of 4 months with normal feed and another group with chlorphentermine for 4-16 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. RESULTS: Chloroquine caused severe lipidosis in the neuroretina and slight photoreceptor cell degeneration after 12 weeks of treatment. The b-wave was reduced to 30% of initial values. After withdrawal the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. The a-wave and b-wave amplitudes were reduced to 25% and 16% of initial values, respectively. Chlorphentermine caused pronounced lipidosis in the pigment epithelium and less numerous in the neuroretina after 16 weeks; no photoreceptor cell degeneration was found. The b-wave was reduced to 80% of initial values, the a-wave appeared unaffected. CONCLUSION: Whether lipidosis is the primary cause of changes in the electroretinogram and of receptor cell degeneration is doubtful. Excessive lipid storage may be the cause of secondary changes. It is unlikely that lipidosis in pigment epithelium played a role.

Administration, Oral↗

PubMed1996

Chloroquine-induced lipidosis in the rat retina: functional and morphological changes after withdrawal of the drug.

BACKGROUND: The antimalarial and antirheumatic drug chloroquine is one of the most infamous amphiphilic cationic drugs in clinical ophthalmology. It is known to cause lipidosis and photoreceptor degeneration in the human and the rat retina. METHODS: We treated female albino Wistar rats (mean weight 200 g) orally with chloroquine (95 mg/kg body weight) for 12 weeks, followed by a period of 4 months with normal feed. After initial electroretinography in all rats, measurements were made after 4 and 12 weeks of treatment and 16 weeks after withdrawal. The rats were prepared for histological examination. RESULTS: Treatment of rats with chloroquine caused severe lipidosis in the neuroretina; photoreceptor cell degeneration was slight. After 12 weeks of treatment, the b-wave amplitude was reduced to 30% of the initial value; the a-wave amplitude was reduced, but remained within the range of normal values. After withdrawal of chloroquine the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. Despite remission of lipidosis, electroretinography demonstrated functional disturbances, marked by reduction of the a- and b-wave amplitudes to 25% and 16% of initial values, respectively. CONCLUSIONS: Seen from the point of view of function, it is doubtful whether lipidosis is the primary cause of changes in the electroretinogram or of receptor cell degeneration.

Animals↗

PubMed1995

Chloroquine-induced lipidosis in the rat retina: a functional and morphological study.

Corneal opacity, reversible retinal lipidosis and irreversible receptor cell degeneration are known to occur after long-term treatment with chloroquine. Female albino Wistar rats (initial age 6 weeks, weight between 100 and 150 g) were treated orally with chloroquine (40-60 mg/kg body weight) for 4 weeks and with 70-80 mg/kg body weight for the following 4 (group A) and 8 weeks (group B). The animals were submitted to electroretinography ERG, and the retinas were prepared for histological investigation. After treatment with chloroquine for 8 weeks, lipidosis-like inclusions could be seen in the rat retina. A deformation of the receptor cell layer was not observed by light microscopy. The a-wave amplitude decreased to 33% and the b-wave amplitude to 40% of the values before treatment. In contrast to group A, we found receptor cell degeneration and macrophage-like cells in the peripheral and central retina in rats treated for 12 weeks. These changes were probably responsible for a-wave and b-wave reductions of 50 and 79% of values before treatment, respectively. It can be assumed that changes in ERG parameters in the first period are caused by lipidosis. Later extremer deformation is induced by receptor cell degeneration and accompanying lipidosis.

Animals↗

PubMed1994

Chlorphentermine-induced lipidosis in the rat retina: a functional and morphological study.

Chronic administration of the cationic amphiphilic anorexigenic drug chlorphentermine to rats has previously been shown to induce extraocular and ocular lipidosis: large numbers of lipidosis-related cytoplasmic inclusions can be found in the pigment epithelium and smaller numbers in the neuroretina. In the present study, female albino Wistar rats were treated orally with chlorphentermine (30-45 mg/kg body weight) for 4-16 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. Our histological findings corresponded to previous reports. The changes in electroretinographic parameters were low. The clearest change was a reduction of the b-wave amplitude of 20% after 12 and 16 weeks of treatment compared with the values before drug treatment. The a-wave amplitude did not differ from that in the control group. Lipidosis in the neuroretina may be the reason for functional influences on the b-wave amplitude. The function of the receptor cells, which is represented by the a-wave, appeared unaffected by chlorphentermine.

Administration, Oral↗

PubMed1994

A new system for recording electroretinographical potentials in animals.

Electroretinography can provide meaningful evidence of oculotoxic changes. We describe a new recording system specially constructed for animal experiments. It meets the standards for electroretinographical investigations and recording systems set up by international committees. The recording apparatus has a resolution of 0.49 microV (amplitude) and 1 ms with a sensitivity range of +/- 1 mV full scale and a band-pass of 0.03 to 1,000 Hz. The signals are digitized and processed by a computer. The calibration symbol is faithfully represented as a rectangular impulse with an amplitude of 100 microV and a period of 100 ms. Normal values were calculated for 25-week-old albino Wistar rats. The normal range is defined as the mean +/- 2 SD for A and B wave parameters. These normal values can serve as reference values for future studies in oculotoxicity.

Animals↗

PubMedDate not supplied

Intraocular microendoscopy: experiments in pig eyes.

A new microendoscope is introduced for intraocular use. The probe diameter measures 0.96 mm. The resolving power is 360,000 pixels. Initial experiments on porcine eyes show the image quality to be excellent. This new endoscope may be helpful in lacrimal duct surgery, in cases of hazy corneas with intraocular pathology, for removal of intraocular foreign bodies, and in the diagnosis of tumors of the ciliary body or orbit.

Animals↗