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141.
Zusammenfassung 1. Das Tauchen als Methode zur Untersuchung von Plankton und Echostreuschichten wird durch vier Beispiele erläutert: (a) Visuelle Beobachtungen an Wasserschichtungen und Grenzschichten durch Schwimmtaucher. (b) Untersuchung von Echostreuschichten durch Freitaucher, wobei sich ergab, daß angesammeltes biogenes Material in den untersuchten Sprung- beziehungsweise Streuschichten die Schallreflektion nicht beeinflußt. (c) Beobachtung von Großplankton und Feststellung von Planktonund Sestonkonzentrationen beim Tauchen mit dem Bathyscaph. (d) Untersuchung der Tiefenstreuschicht (deep scattering layer) durch Beobachtung der Vertikalwanderung bestimmter Arten des Großplanktons mit den Tauchbooten Bathyscaph und Soucoupe Plongeante. Physonectide Siphonophoren und Myctophiden standen in deutlicher Beziehung zur Tiefenstreuschicht und wurden als Echogeber erkannt.2. Die Möglichkeiten, von Tauchbooten aus quantitative und qualitative Proben von Plankton und auch vom Benthos zu nehmen, sind zur Zeit noch unzureichend. Die Entwicklung entsprechender Geräte für den wahlweisen und mehrfachen Einsatz bei demselben Tauchgang wird empfohlen.
Diving observations on plankton and on scattering layers
Diving techniques are employed as a research tool in plankton investigations carried out in shallow water of the western Baltic Sea. Observations and samplings were made by skin divers on scattering layers corresponding to the discontinuity layers. Biogene materials, sometimes concentrated at the thermocline, are not responsible for this special kind of scattering, but rather discontinuity of salinity and temperature (Lenz 1965). For observations in deep water the use of undersea vehicles is recommended. From the Bathyscaph and the diving saucer, single plankton organisms and plankton concentrations were observed (e. g.Bernard 1958); investigations on the deep scattering layer have shown physonectid siphonophores and myctophids to be scatterers (Barham 1966). The equipment for sampling plankton and benthos from undersea vehicles is poorly developed. We need urgently gear for quantitative and qualitative sampling and for manifold use during single dives, i. e., multiple sampling gear and magazins for storage of samples.
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Changes in tension of spiral strips from canine and human veins induced by various drugs are compared with results from the literature on human veins. The order of potencies of alpha-adrenoceptor stimulating amines (adrenaline greater than noradrenaline greater than dopamine greater than isoprenaline) is similar in human and canine veins. Comparison of the affinities for alpha-adrenoceptors of pharmacologic drugs (thymoxamine, indoramine, clonidine, dihydroergotamine) suggest marked differences between the alpha-adrenoceptors in veins from man and dog. Venoconstriction mediating 5-HT receptors and a very small population of beta-adrenoceptors exist in both species. Human veins are always dilated by histamine, while canine femoral veins in vitro are relaxed by lower and contracted by higher histamine concentrations. Prostaglandin F2 alpha constricts both canine femoral and human hand veins. PGA2 and PGE2 increase the tension of canine and human veins in vitro but dilate human hand veins in situ. The order of potencies of ergot alkaloids in canine femoral veins is ergotamine greater than dihydroergovaline greater than dihydroergotamine = dihydroergostine greater than methysergide, whereas in human hand veins it is ergotamine = dihydroergovaline greater than methysergide greater than dihydroergotamine greater than dihydroergostine. In dogs the venoconstrictor effect of ergotamine is mediated by at least 3 mechanisms: stimulation of [1] alpha-adrenoceptors, [2] 5-HT receptors and [3] endogenous prostaglandin synthesis. Stimulation of alpha-adrenoceptors by dihydroergotamine and of 5-HT receptors by ergotamine was confirmed on human hand veins in situ. Prejunctional receptors at sympathetic nerve terminals are involved in the regulation of venous tone. Inhibitory alpha-adrenoceptors, dopamine and PGE2 receptors as well as facilitating beta-adrenoceptor existing at human vasoconstrictor nerves may be stimulated or blocked by pharmacologic drugs thereby modifying venous tone.  相似文献   
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The nature of the conversion of thyroxine (T4) to triiodothyronine (T3) and reverse triiodothyronine (rT3) was investigated in rat liver homogenate and microsomes. A 6-fold rise of T3 and 2.5-fold rise of rT3 levels determined by specific radioimmunoassays was observed over 6 h after the addition of T4. An enzymic process is suggested that converts T4 to T3 and rT3. For T3 the optimal pH is 6 and for rT3, 9.5. The converting activity for both T3 and rT3 is temperature dependent and can be suppressed by heat, H2O2, merthiolate and by 5-propyl-2-thiouracil. rT3 and to a lesser degree iodide, were able to inhibit the production of T3 in a dose related fashion. Therefore the pH dependendy, rT3 and iodide may regulate the availability of T3 or rT3 depending on the metabolic requirements of thyroid hormones.  相似文献   
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An injection of cortisone acetate at a dose of 5 mg/100 g body weight concomitant with dibutryl cyclic AMP prevents the increase in the activity of rat liver cytosol serine aminotransferase (L-serine: pyruvate aminotransferase, EC 2.6.1.51) elicited by the nucleotide with a lag of about 2 h. If the glucocorticoid is given 2 h prior to the nucleotide inducer, the lag disappears. The inhibitory effect of cortisone acetate gradually decays and is no longer detectable 12 h following its administration. Theophylline, insulin and glucose at doses which affect significantly the level of tyrosine aminotransferase, have no effect on the level of serine aminotransferase and on the cortisone inhibition. The inhibitory effect of the glucocorticoid on the dibutyryl cyclic AMP-mediated increase in serine aminotransferase diminishes with the age of animals. Increase in the enzyme activity by a single dose of glucagon can also be inhibited by cortisone acetate and actinomycin D as in the case with dibutyrl cyclic AMP as an inducer. The possibility of the existence of a specific inhibitory factor which is formed in response to cortisone acetate is discussed.  相似文献   
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