Stress Analysis of Circular Frames

The stresses in circular frames of constant bending stiffnesses, as encountered in thin-wall shells, are investigated from the point of view of finite depth of sectional area of frame. The solution is carried out for four fundamental load conditions. The method is illustrated on a worked out example

Zur Diagnostik des Diabetes insipidus unter besonderer Berücksichtigung hypophysektomierter Patienten

Verschiedene, am gleichen Patienten durchgeführte Stimulationsteste für die ADH-Sekretion (17-Std.-Durstversuch, Carter-Robbins-Test, osmotische Diurese) zeigen eine ausgezeichnete Korrelation. Auf Grund dieser Ergebnisse werden Richtlinien zur möglichst einfachen Diagnostik einer Konzentrationsstörung vorgeschlagen. In den meisten Fällen kann allein schon auf Grund eines exakt durchgeführten Durstversuchs eine Konzentrationsstörung nachgewiesen (höchste Urinosmolalität 750 mOsm/kg) werden. Lediglich bei einer höchsten Urinosmolalität im 17-Std.-Durstversuch zwischen 500 und 750 mOsm/kg müssen aufwendigere und den Patienten mehr belastende Tests (z. B. Carter-Robbins-Test) eingesetzt werden, um das Vorliegen bzw. den Grad einer Konzentrationsstörung endgültig diagnostizieren zu können. ADH-Injektionen dienen dabei zur Differenzierung zwischen einem ADH-Mangel und einer mangelhaften ADH-Ansprechbarkeit der Niere. Unsere Untersuchungen an hypophysektomierten Patienten (N=29) zeigen auch bei Patienten ohne polyurisch-polydiptisches Syndrom (N=22) eine gegenüber Normalpersonen signifikant eingeschränkte Konzentrationsleistung im 17-Std.-Durstversuch.The results of three different stimulation tests for ADH (17 hours thirst period, Carter-Robbins-test, osmotic diuresis) correlate well in the same patient. Because of this we propose a simplified procedure for the detection of failure to produce a concentrated urine. In most cases merely on the basis of a precisely executed thirst period test, one can either recognize an abnormality of concentration (highest urine osmolality less than 500 mOsm/kg), or exlude it (highest urine osmolality greater than 750 mOsm/kg). Only when the highest urine osmolality lies between 500 and 750 mOsm/kg after a 17 hour thirst must more painstaking tests (e.g. Carter-Robbins test) be employed to determine both the presence of and the degree of a failure to produce a concentrated urine. An injection of ADH can be used to differentiate between a deficiency of ADH and a defective response of the kidneys to ADH. Our investigations on hypophysectomized patients (n=29) showed that also in patients without the syndrome of polyuria-polydypsia (n=22), there was a significantly reduced capacity to concentrate urine during a 17 hour thirst period, as compared with normal people

Attenuation of Mammary Gland Dysplasia and Feeding Difficulties in Tabby Mice by Fetal Therapy.

Hypohidrotic ectodermal dysplasias (HED) are hereditary differentiation disorders of multiple ectodermal structures including the mammary gland. The X-linked form of HED (XLHED) is caused by a lack of the secreted signaling molecule ectodysplasin A1 (EDA1) which is encoded by the gene EDA and belongs to the tumor necrosis factor (TNF) superfamily. Although male patients (hemizygous) are usually more severely affected by XLHED, heterozygous female carriers of an EDA mutation may also suffer from a variety of symptoms, in particular from abnormal development of their breasts. In Tabby mice, a well-studied animal model of XLHED, EDA1 is absent. We investigated the effects of prenatal administration of Fc-EDA, a recombinant EDA1 replacement protein, on mammary gland development in female Tabby mice. Intra-amniotic delivery of Fc-EDA to fetal animals resulted later in improved breastfeeding and thus promoted the growth of their offspring. In detail, such treatment led to a normalization of the nipple shape (protrusion, tapering) that facilitated sucking. Mammary glands of treated female Tabby mice also showed internal changes, including enhanced branching morphogenesis and ductal elongation. Our findings indicate that EDA receptor stimulation during development has a stable impact on later stages of mammary gland differentiation, including lactation, but also show that intra-amniotic administration of an EDA1 replacement protein to fetal Tabby mice partially corrects the mammary gland phenotype in female adult animals