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Biomedical subjects

F Koch

Publications and source records attributed to F Koch.

At least 91 records · Page 5Linked to original sources
PubMed1991

[Delayed resorption of subretinal fluid after pneumatic retinopexy].

Delayed resorption of pooled subretinal fluid has been reported to cause impaired visual acuity due to involvement of the macula in up to 10% of all case. In our series of 60 eyes treated consecutively with pneumatic retinopexy for retinal detachment, 9 eyes experienced delayed absorption of subretinal fluid. Only 6 eyes showed the phenomenon of pooled, localized subretinal fluid without peripheral extension to the ora serrata. The time for complete absorption of these circumscribed subretinal bullae ranged from 8 to 52 weeks (mean 22.7 weeks). Impaired visual acuity could not be detected in any of these cases. This may be due to the location of these bullae, which never involved the macula. Therefore, we do not consider the occurrence of this phenomenon to be a reason not to carry out pneumatic retinopexy.

Adult↗
PubMed1991

[Development of lens opacities in a period of 6 months after pneumatic retinopexy].

When performing a pneumatic retinopexy, air or gas is injected into the vitreous cavity to reattach a primary, rhegmatogenous retinal detachment. SF6 gas, for examples, remains in the vitreous cavity for up to 2 weeks before it is completely absorbed. It is conceivable that the injection of SF6 gas into the vitreous cavity interferes with lens metabolism, thus causing opacities of the lens. Even minor early changes in lens transparency can be monitored by Scheimpflug photography. Two months after performing a pneumatic retinopexy, 31 out of 100 consecutive eyes showed a loss of lens transparency, which was not pronounced or statistically significant. Six months after surgery the loss of transparency was more pronounced in all lens layers, increasing from the front to the back. The increment was statistically significant for the anterior lens cortex. Further investigations are needed to determine whether lens changes are the result of the intraocular tamponade with SF6 gas or are related to other factors, such as the surgical maneuver itself.

Cataract↗
PubMed1990

Disappearance of certain acidic organelles (endosomes and Langerhans cell granules) accompanies loss of antigen processing capacity upon culture of epidermal Langerhans cells.

Freshly isolated epidermal Langerhans cells (LC) can actively process native protein antigens, but are weak in sensitizing helper T cells. During culture, when LC mature into potent immunostimulatory dendritic cells, T cell sensitizing capacity develops but antigen processing capacity is downregulated. Processing of exogenous antigens for class II-restricted antigen presentation involves acidic organelles. We used the DAMP-technique to monitor acidic organelles at the ultrastructural level in fresh, as well as cultured, mouse and human LC. We observed that the loss of antigen processing capacity with culture of LC was reflected by the disappearance of certain acidic organelles, namely endosomes (particularly early ones), and the hitherto enigmatic LC granules ("Birbeck Granules"). Our findings support the notion that endosomes are critical for antigen processing and suggest that LC granules might be involved as well.

Animals↗
PubMed1990

Tumor necrosis factor alpha maintains the viability of murine epidermal Langerhans cells in culture, but in contrast to granulocyte/macrophage colony-stimulating factor, without inducing their functional maturation.

Freshly isolated murine epidermal Langerhans cells (LC) are weak stimulators of resting T cells but increase their stimulatory capacity 10-30-fold upon 2-3 d of culture together with other epidermal cells. This maturation of LC is mediated by two keratinocyte products. Granulocyte/macrophage colony-stimulating factor (GM-CSF) maintains viability and increases function. IL-1 alone does not keep LC alive, but when combined with GM-CSF further enhances their stimulatory activity. We have now searched for a cytokine that would keep LC in a viable, but functionally immature state. When LC (enriched to greater than 75%) were cultured in the presence of GM-CSF (2 ng/ml) or murine (TNF-alpha) (plateau effect at 62 U/ml), the recovery of viable LC after 72 h was identical. The LC cultured in murine TNF-alpha, however, were 10-30 times less active in stimulating resting T cells. A series of experiments demonstrated that this phenomenon was not due to the induction of insufficient amounts of GM-CSF, the induction of a suppressor factor, or a toxic effect of TNF-alpha. Interestingly, the observed TNF-alpha activity exhibited a species preference, as human TNF-alpha was not active at comparable doses. We have observed an unexpected effect of TNF-alpha on LC in vitro. Though we found that freshly prepared epidermal cells express TNF-alpha mRNA, further studies are needed to establish whether TNF-alpha plays a role in vivo by keeping resident LC in a viable, but functionally immature state.

Animals↗
PubMed1990

Ultrastructural pathology of anterior persistent hyperplastic primary vitreous.

Using transmission electron microscopy, the fine structure of anterior persistent hyperplastic primary vitreous (PHPV) removed from the eyes of four infants was studied. The tissue mass was composed of vessels derived from or representing the tunica vasculosa lentis posterior and the vasa hyaloidea propria. They were embedded in a loose connective-tissue matrix containing many fibroblasts and mature collagen fibrils. Toward the posterior surface, the fibroblasts became more numerous, elongated and densely packed. At the point of its entry into the posterior pole of the mass, the hyaloid artery was found to be surrounded by glial cells, probably representing an extension of the wall cells of the hyaloid canal. Venous drainage of the PHPV nodules seemed to occur via the ciliary body to which they were connected by tiny vessels bridging the distance from the PHPV lump to elongated ciliary processes. The anterior surface of the tissue lump was covered with lens fragments. These remnants showed signs of very early disturbance of lens development, with a failure to form posterior lens fibers. Based on these findings, the authors suggest that PHPV may be secondary to a primary defect in lens development.

Eye Diseases↗
PubMed1990

Primary structure of rat RT6.2, a nonglycosylated phosphatidylinositol-linked surface marker of postthymic T cells.

RT6 is an unusual cell membrane protein that is expressed exclusively by postthymic T cells. The inherent defect in its expression has been correlated to lymphopenia and genetically determined susceptibility for insulin-dependent diabetes mellitus in the rat. We report here the primary structure of the RT6.2 alloantigen as deduced from the cDNA sequence. The predicted amino acid sequence of RT6.2 begins with a conventional leader of 20 amino acids and ends in a hydrophobic C-terminal extension peptide of 29 amino acids as is common for phosphatidylinositol-anchored proteins. Native RT6.2 is predicted to comprise 226 amino acids, with a calculated Mr of 26,036. Four cysteine residues account for two intrachain disulfide bonds. The sequence lacks potential N-glycosylation sites and contains an excess of positively charged residues. Homology searches in protein sequence data banks suggest that RT6.2 is not encoded by a member of the immunoglobulin supergene family. Moreover, these analyses did not reveal any close homologies of RT6.2 to known proteins: the highest homology found was 21.2% identity in a 52-amino acid overlap to the torpedo acetylcholinesterase precursor. Southern blot analyses indicate that RT6.2 is the product of a single-copy gene and provide evidence for closely related genes in the mouse and other species. The corresponding gene products remain to be identified.

Amino Acid Sequence↗
PubMed1990

Dendritic cell production of cytokines and responses to cytokines.

Dendritic cells (DC) are a family of bone marrow-derived MHC class II expressing cells which occur in small numbers in most lymphoid and nonlymphoid tissues. They represent a distinct lineage of leukocytes which can be found in two distinct maturational stages: immature dendritic cells are exemplified by the Langerhans cells in the epidermis, and are considered to be precursors to the mature dendritic cells in the lymphoid organs. These maturational stages can be distinguished by phenotypic and functional characteristics. Immature dendritic cells are weak stimulators of resting T lymphocytes but are excellent in processing soluble protein antigens for presentation to T cell clones. Mature dendritic cells show exactly reciprocal features. In this review the relatively few available data on cytokine production by DC and responses of DC to cytokines are collected. Our goal is to consider the role of cytokines in DC function including the transition from immature to mature stages.

Animals↗
PubMed1990

Comparison of Scheimpflug-photography, specular microscopy and scanning electron microscopy to detect corneal changes in toxicity studies in rats.

With an increasing number of in-vivo methods to examine the eyes of laboratory animals, the rat has become an important animal model in experimental eye research. Specular microscopy is a clinical tool to examine the corneal endothelium in-vivo. To evaluate the versatility of this method for small animal eyes, we studied both corneal endothelial cell-count and corneal thickness in normal rats as well as those with diabetic, naphthalene and UV-B cataract. As a reference scanning electron microscopy (SEM) of the corneal endothelium was performed. For cell-counts the correlation coefficient between both methods was found to be sufficient. The comparison of corneal thickness measurement (SEM-values) with specular microscopy and with Scheimpflugbiometry failed to show a satisfactory correlation. The study proves that specular microscopy is a useful tool to document changes also in the endothelium of the rat-cornea.

Animals↗
PubMed1989

Retinal wound healing after surgical contusion injury.

The lesion was caused by a compression injury to the retina with a vitrectomy instrument in a rhesus monkey; the lesion was examined by electron microscopy 8 years later. The inner surface of the choroid was lined by a layer of cells with the characteristics of fibroblasts. The choriocapillaris was missing. Bruch's membrane was extremely thickened and showed numerous changes. In the center of the scar, the retinal pigment epithelium was discontinuous. The neuroretinal portion of the scar was composed of distorted and dislocated nerve cells, nerve fibers, and glial elements that were probably Müller cells. Towards the vitreous cavity, the surface of the scar contained numerous microvillous processes. A band of zonulae adherentes resembling the outer limiting membrane was seen immediately adjacent to the surface. No inner limiting membrane was seen in the entire scar area.

Animals↗
PubMed1989

The cytotoxic effects of estradiol-17 beta, catecholestradiols and methoxyestradiols on dividing MCF-7 and HeLa cells.

In this study the cytotoxic effects of high concentrations (greater than or equal to 1 x 10(-6) M) of estradiol-17 beta (E2), 2-/4-hydroxyestradiol-17 beta (2-/4-OHE2) and 2-/3-/4-methoxyestradiol-17 beta (2-/3-/4-MeOE2) were determined on dividing MCF-7 and HeLa cells. The 2-MeOE2 metabolite followed by 2-OHE2 and E2 (in this order) proved to be extremely toxic to dividing MCF-7 and HeLa cells. The cytotoxic effect on these cells comprised uneven chromosome distribution. Indirect immunofluorescent studies, in which monoclonal anti-alpha-tubulin antibodies were used, showed that these compounds (2-MeOE2 greater than 2-OHE2 greater than E2) at high concentrations caused abnormal and fragmented polar formations as well as disorientated microtubule arrangement in the dividing MCF-7 and HeLa cells. The 4-OHE2 and 3-/4-MeOE2 metabolites had little or no cytotoxic effects on dividing cells. The large number of abnormal metaphases seen in HeLa cells exposed to 2-MeOE2 suggested that this metabolite may be the ultimate cytotoxic compound. The reduction in the number of HeLa cells with abnormal metaphase configurations after exposure to 2-OHE2 plus quinalizarin (an inhibitor of catechol-O-methyltransferase) indicated that the production of 2-MeOE2 is necessary for the formation of abnormal spindles in metaphase. Quinalizarin treatment in the presence of 2-MeOE2 had no effect on the large number of abnormal metaphases. We therefore conclude that neither E2 nor 2-OHE2, but a high concentration of 2-MeOE2 is responsible for abnormal spindle formation. In additional experiments the number of normal and abnormal dividing HeLa cells were greatly reduced when simultaneously exposed to E2 and 2-/4-hydroxylase-inhibitor alpha-naphthoflavone.

Benzoflavones↗