WNT10A variants: following the pattern of inheritance in tooth agenesis and self-reported family history of cancer

Clinical Oral Investigations - The aim of this study was the analysis of WNT10A variants in seven families of probands with various forms of tooth agenesis and self-reported family history of...     

Contractile and endothelium-dependent dilatory responses of cerebral arteries at various extracellular magnesium concentrations

To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10(-8)-10(-5) M norepinephrine, were significantly potentiated at low Mg2+ (0.8 mM v. the normal, 1.2 mM). High (1.6 and 2.0 mM) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 10(-8)-10(-5) M acetylcholine were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.     

A contribution to the comparison of the efficacy of radiotherapeutic procedures in cervical carcinoma.

This paper presents a new method in which the regression velocity of cervical carcinoma is measured by computer tomography and the results evaluated by two statistical methods: non-linear regression analysis and survival analysis. By means of this approach it was possible to compare the early effect of therapy in patients treated with intracavitary application of 226Ra plus external radiotherapy with those treated with 252Cf, 226Ra and extended radiotherapy. In the latter group a higher efficacy of the therapy was demonstrated by both statistical methods. As the timing between external and intracavitary radiotherapy was different in the two groups and as 252Cf contributed to a rather small part of the total radiation dose it could not be concluded that the difference in efficacy really was due to 252Cf. Of essential interest was, however, that an obvious difference in efficacy could be found between two slightly different treatment techniques. The statistical procedure called survival analysis, used here parallelly with weighed regression analysis seemed to give better results than a classical regression analysis and can thus be recommended for processing of clinical data of the type which is discussed in this paper.     

The neurosensory musculocutaneous tensor fasciae latae flap: long term results.

In 1971 we started covering pressure sores and unstable scars with transposition-rotation-muscle and musculocutaneous flaps. In 1980 we published the first results with 6 neurosensory musculocutaneous tensor fasciae latae flaps. Until April 1989, 31 tensor fasciae latae flaps (TFL) were used, and we review a consecutive series of 19 neurosensory TFL-flaps. Questions such as whether to delay the procedure; early and late complications; evolution of the sensation; and indications are outlined under the aspects of long term follow up studies. The conclusion is that if the neurological pattern permits a neurosensory flap, such flaps should be done because no local recurrence occurred. In extended neurosensory TFL-flaps sensation of the filling status of the rectum is improved, and sitting control and perception of the 'body scheme' are also improved.     

The electrically stimulated (dynamic) graciloplasty for faecal incontinence — first experiences with a modified muscle sling

Continence following the gracilis stimulated neosphincter reconstruction after total rectal excision is inferior to that obtained in the presence of an intact anal canal. We describe a modification of the alpha loop in which the tendon is brought through the belly of the gracilis muscle. The results in three patients are presented.

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Résumé La reconstruction sphinctérienne après excision totale du rectum au moyen d'un néosphincter fait d'un muscle gracilis stimulé donne des résultats sur le plan de la continence inférieurs à ceux obtenus en présence d'un canal anal intact. Nous décrivons une modification de l'anse alpha dans laquelle le tendon est fixé après avoir traversé la sangle de muscle gracilis. Les résultats de trois patients sont rapportés.

     

Anthracycline-induced cardiotoxicity: Overview of studies examining the roles of oxidative stress and free cellular iron

The risk of cardiotoxicity is the most serious drawback to the clinical usefulness of anthracycline antineoplastic antibiotics, which include doxorubicin (adriamycin), daunorubicin or epirubicin. Nevertheless, these compounds remain among the most widely used anticancer drugs. The molecular pathogenesis of anthracycline cardiotoxicity remains highly controversial, although the oxidative stress-based hypothesis involving intramyocardial production of reactive oxygen species (ROS) has gained the widest acceptance. Anthracyclines may promote the formation of ROS through redox cycling of their aglycones as well as their anthracycline-iron complexes. This proposed mechanism has become particularly popular in light of the high cardioprotective efficacy of dexrazoxane (ICRF-187). The mechanism of action of this drug has been attributed to its hydrolytic transformation into the iron-chelating metabolite ADR-925, which may act by displacing iron from anthracycline-iron complexes or by chelating free or loosely bound cellular iron, thus preventing site-specific iron-catalyzed ROS damage. However, during the last decade, calls for the critical reassessment of this “ROS and iron” hypothesis have emerged. Numerous antioxidants, although efficient in cellular or acute animal experiments, have failed to alleviate anthracycline cardiotoxicity in clinically relevant chronic animal models or clinical trials. In addition, studies with chelators that are stronger and more selective for iron than ADR-925 have also yielded negative or, at best, mixed outcomes. Hence, several lines of evidence suggest that mechanisms other than the traditionally emphasized “ROS and iron” hypothesis are involved in anthracycline-induced cardiotoxicity and that these alternative mechanisms may be better bases for designing approaches to achieve efficient and safe cardioprotection.