Search PubMed⌕ Search

Biomedical subjects

G Mahrle

Publications and source records attributed to G Mahrle.

At least 145 records · Page 8Linked to original sources

[Lip carcinoma and its surgical treatment].

Cancer of the lip occurs in about 90 percent at the lower lip arising in the vermilion mucosa. In tumor stage I the type of repair depends on the size of the primary tumor. Small tumors are best treated by a simple full-thickness W-excision with direct closure, occasionally combined with vermilionectomy. The simple W-excision is the most common procedure in lip cancer (65%). After excision of greater tumors, repair may be performed by cross lip flap of the Estlander-Abbe type or by the fan-flap of the Gillies type. Large defects are closed with Dieffenbach's or Burow's flap. The Burow's technique give better cosmetic and functional results than the Dieffenbach's method. Also in comparison to the cross lip flaps Burow's technique advantages. The orificium of the mouth remains wide, the lateral angle is not distorted and the tumor may be removed with a broad margin in the normal tissue. Therefore, the Burow's technique is frequently applied (30%) displacing the other methods(is less than 5%). At least the practice of two techniques may be sufficient in dermato-surgery, the W-excision with or without vermilionectomy; and the Burow's technique with its modifications.

Adult↗

Intramembraneous particles and transmembraneous ionic channels in the epidermal cell membrane. A cytochemical study with the alcian blue-lanthanum technique.

Normal skin was investigated with the Alcian blue-lanthanum technique. Nexus (gap junctions) were found in the stratum Malpighii. They were less numerous in the basal layer, increasing to the upper layers of the epidermis and lacking in the stratum corneum. They were five-layered, about 20 nm thick and showed a 5-7 nm broad lanthanum positive intercellular dense line. Transitional forms between the narrow intercellular space and the real nexus were observed. These "nearly nexus" were broader, the intercellular dense line measured 6-15 nm, and sometimes they were seven-layered. Both, nexus and "nearly nexus" revealed a specific distribution of lanthanum in their membranes. Lanthanum ions seemed to penetrate the membranes forming electron-dense transversal channels branching off from the central dense line with a periodicity of 3 nm. The tangential sections suggested that this distribution was based on the aggregation of intramembraneous particles 1.5-2.0 nm in diameter, which in some areas may be gathered to greater subunits. The nexus may play a role in the control of epidermal proliferation.

Alcian Blue↗

[Disturbed distribution of surface glycoconjugates of the plasma cell membrane in psoriasis. Cytochemical detection using the alcianblue-lanthan-reaction (author's transl)].

Lanthanum has been used as a tracer for the intercellular space and the surface coats in different epithelia including human epidermis, however, lanthanum compounds may or may not penetrate into skin specimes and reaction product may or may not be present in the intercellular space. After treatment with alcian blue prior exposure to lanthanum the trilaminar plasma membrane was more regularly stained and a thin coat of reaction product corresponding to superficial glycoconjugates outlined the cell surface and filled the narrow intercellular space in normal epidermis. In psoriatic epidermis the quantity of superficial membrane-bound glycoconjugates was rather reduced, their distribution and compartmentalization was profoundly changed and the outer leaflet of the trilaminar plasma membrane was not always clearly seen, having a "moth-eaten appearance" in some places. These findings show once more that alterations of the cell membranes and their surface architecture are present in psoriasis. They may play a major role in the pathogenesis of the disease, influencing the activities of membrane-bound enzymes and the flow of the epidermal growth control mechanism. The glycocalyx may serve in this mechanism as an accumulator of energy rich compounds or as a receptor site of membrane-bound ezymes. According to our views it represents a "ground substance" of epidermal origin, which controls the social behaviour of the keratinocytes in tissue.

Adult↗

Localization and activity of tissue bound cyclic nucleotide phosphodiesterase in normal and lack of changes in psoriatic human skin.

This study has been undertaken to elucidate the localization and the activity of cyclic nucleotide phosphodiesterase (PDE) in psoriatic epidermis compared to normal. The results showed that the evaluation of cytochemical methods may be difficult because of the various factors which interfere with the reaction and the considerable amount of background staining. Additionally, only the tissue bound particulate enzyme fraction may be demonstrated by cytochemical means. Nevertheless, the method did reveal that the activity of PDE, if any, is localized on the cytoplasmic membranes of the cells, independent of their origin, and not on the cell surface. Moreover, no differences were found between normal and psoriatic skin. It seems, therefore, that the intracellular degradation of cAMP remains unaltered in psoriasis.

Humans↗

[Lack of beta-adrenergic stimulation of membrane bound adenyl cyclase in psoriasis as compared to normal epidermis (author's transl)].

Glucagon and beta-adrenergic compounds such as 1-isoproterenol stimulated the low activity of an ATP-utilizing enzyme located on the cell membranes of normal keratinocytes. Addition of beta-antagonist propranolol to the incubation medium prevented the stimulatory effect of 1-isoproterenol. We considered, therefore, the reaction product being due to epidermal membrane-bound adenyl cyclase activity. In psoriatic epidermis the basal adenyl cyclase activity was low, similar to normal epidermis, however, glucagon and 1-isoproterenol failed to stimulate the enzyme activity in psoriasis under the same conditions. It seems, therefore, that the beta-adrenergic-cAMP cascade as a regulatory epidermal control mechanism of induced proliferation is ineffective in this disease.

Adenylyl Cyclases↗

Ultrastructural localization and differentiation of membrane-bound ATP utilizing enzymes including adenyl cyclase in normal and psoriatic epidermis.

The total membrane-bound ATP hydrolytic activity in human epidermis is due to the activities of at least three differently located enzymes, namely Mg++-activated ATPase, phosphomonoesterase and adenyl cyclase. Cytochemical studies on psoriatic epidermis with various inhibitory and stimulatory substances showed reduced activities of ATPase and phosphomonoesterase, and a lack of sensitivity of adenyl cyclase to specific stimulators such as isoproterenol and glucagon. Since no differences of basal adenyl cyclase activity were observed between normal and psoriatic human skin without stimulation, it seems likely that in psoriasis a latent defect of adenyl cyclase may exist, resulting in a deficient response of this enzyme to regulatory agents. In conclusion, the present study reveals that not a single enzyme but the entire membrane-bound nucleotide metabolism is altered in psoriatic keratinocytes, causing a disturbance of the membrane-bound energy utilization, similar to findings in proliferating tumour cells.

Adenosine Triphosphatases↗

[Membrane defect as a basic disorder of the growth control mechanism in psoriasis pathogenetic concept and therapeutic consequences (author's transl)].

The system glycocalyz - membrane bound enzymes - cAMP may be regarded as a regulatory mechanism for the control of epidermal growth. The glycocalyz of the epithelial cell membrane is obviously a receptor and accumulator for agents stimulating adenyl cyclase and other membrane-bound enzymes of energy utilisation; cAMP, on the other hand, serves as an intracellular 'mediator' between proliferative stimuli and the DNA of the keratinocytes. Numerous cytological, cytochemical, and enzymatic biochemical studies indicate that this mechanism is profoundly disturbed in psoriasis, particularly at the membrane-bound stage.

Adenylyl Cyclases↗