Brutbiologie des Turmfalken (Falco tinnunculus): 16j?hrige Untersuchungen in Westfalen

Zusammenfassung Anhand einer 16jährigen Untersuchung im Raum Ostwestfalen/Bielefeld wird der Bruterfolg des Turmfalken anhand von 439 Gelegen und 2256 Eiern beschrieben. Drei Brutplatztypen können unterschieden werden: A. Baumbruten in Nestern; B₁. Baumbruten in Nistkästen; B₂. Gebäudebruten in Nischen oder Nistkästen. Zwischen Baumbruten (A) und Nistkastenbruten (B_1/2) werden signifikante Unterschiede beschrieben, die für Nistkästen größere Gelege (ca. ein Ei mehr) und größeren Ausfliegeerfolg belegen. Zwischen Nistkästen in Bäumen (B₁) oder an Gebäuden (B₂) konnten keine signifikanten Unterschiede festgestellt werden. Weiterhin werden Lege- und Schlupftermine, Legerhythmus und oologische Daten aus dem Untersuchungsgebiet angegeben.

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Breeding biology of Kestrels (Falco tinnunculus) in Eastern Westfalia 1972–1987

Summary The 16 years of study gave 439 clutches with 2,256 eggs. We separated three types of breeding sites: the use of (a) stick nests, mostly built by corvids (cf. Tab., Fig. 3), (b₁) nest boxes attached to trees or telegraph poles (Fig. 2) and (b₂) nest boxes or cavities at or in buildings (Fig. 1). Within these different types of breeding places we found some significant differences. Stick nests had less eggs and though less breeding success, which was possibly caused by predation of corvids, especially magpies. Within the two types of places with nest boxes no significant differences could be established. We concluded, that stick nests were marginal in Kestrels and nest boxes were optimal despite of their placement in trees, at poles or in buildings. Furthermore, the timing of breeding cycle was described (Fig. 4) and laying interval was determind to an average value of approximately two days (Fig. 5). Mean egg size was and average volume 21.2 cm². Two daily controlled clutches lost 15.5% and 16.1% of mass (Fig. 6) pressumably mostly due to water losses.

     

The influence of fixation on the relative amount of cytoplasmic ribosomes in mouse epidermal basal keratinocytes

The nature and significance of so-called dark keratinocytes in the epidermis during chemical carcinogenesis is still a matter of concern and debate. Based on ultrastructural observations it has been suggested that dark cells most often are shrunken cells. Reports on skin carcinogenesis, however, claim that dark cells are a sign of ongoing tumor promotion and represent those stem cells in the epidermis from which the tumors originate. It is therefore important to find out whether these cells are simply injured and shrunken cells, or vital cells of great importance for carcinogenesis. Dark cells are assumed to be rich in ribosomes. There is evidence, however, that the observed number of dark cells is highly dependent on tissue fixation. In the present ultrastructural study, morphometric methods were used to compare the effects of two different fixation procedures on the amount of cytoplasmic ribosomes in dark cells from both untreated and carcinogen-treated hairless mouse epidermis. The results show that the ultrastructural features of both dark and clear cells vary considerably with different fixation procedures. In acetone-treated controls typical dark cells are only observed when the fixative has a lower osmotic activity than the plasma. With iso-osmolal fixation typical dark cells are not observed. After an abortive two-stage carcinogenesis treatment, in which a single application of 9,10-dimethyl-l,2-benzanthracene (DMBA) in acetone was followed by a single application of 12-O-tetradecanoyl-13-acetate (TPA) in acetone, signs of cell injury could be found after both fixation procedures. With DMBA/TPA and hypo-osmolal fixation the number of dark cells seemed to increase, whereas only signs of cell injury with occurrence of some heavily altered “clear cells” dominated the picture with iso-osmolal fixation. Morphometry showed that both the numerical and the volumetric densities of cytoplasmic ribosomes in basal keratinocytes varied most significantly with the fixation procedure used. The cytoplasmic volumes did not vary in a way that could explain these differences. One might therefore assume that the number of ribosomes depends on the fixative. Large swelling artifacts occurred when a fixative with low osmotic activity was used, leading to compression of neighboring cells. Hence, an increased ribosomal density reported previously in dark cells is probably related to such cell volume artifacts and does not reflect an actually increased quantity of ribosomes. With both fixation procedures, a single application of DMBA followed by one of TPA appeared to produce an increased number of ribosomes in basal keratinocytes. When hypo-osmolal fixation was used, however, treatment with DMBA/TPA did not influence the cytoplasmic volume or the numerical density of ribosomes, in dark cells. This might indicate that so-called dark keratinocytes following DMBA/TPA treatment are functionally inactive cells that appear more vulnerable than active cells to compression during hypo-osmolal fixation.     

The effects of polyinosinic:polycytidylic acid (pI:C) on the graft-vs-host (GVH) reaction. II. Increased NK-mediated rejection on C57BL/6 lymphocytes by (C57BL/6 X A)F1 mice

We previously demonstrated that treatment of (C57BL/6 X A)F1 (F1) recipient mice with polyinosinic:polycytidylic acid (pI:C) before injection with 30 X 10(6) C57BL/6 (B6) lymphocytes prevents both the immunosuppression and pathologic lesions typical of graft-vs-host (GVH) reactions. We now report the further characterization of this phenomenon. Donor spleen and lymph node cells were labeled with fluorescein in vitro and injected into pI:C-treated or untreated mice. Two days later, recipient splenocytes were analyzed for the presence of fluorescein-labeled donor cells by flow microfluorometry. Treatment of F1 mice with pI:C resulted in a sharp reduction in the recovery of labeled B6 but not A strain parental cells. Treatment with pI:C had no effect when syngeneic recipients were used, or when F1 cells were injected into A, B6, or F1 recipients. These results suggest that pI:C treatment induces rejection of B6 but not A or F1 lymphocytes by F1 hybrid mice at least as early as 2 days after donor cell transfer. As F1 cells are not rejected by either parent, rejection does not seem to be directed against classical alloantigens. These observations are compatible with the previously described model of hybrid resistance (HR) against bone marrow grafts. The rapidity of rejection strongly suggested that natural cytotoxic mechanisms were involved, thus, natural killer (NK) cell and macrophage (M phi) cytotoxic activities were tested throughout the time when the parental cell graft was being rejected. Over this period, pI:C treatment increased cytotoxic activity against the NK-sensitive target cell line YAC-1 but had no effect on spontaneous M phi tumoricidal activity against the L5178Y and MDAY-D2 cell lines. The results suggest that NK cells, but not M phi, may be involved in the elimination of B6 parental cells by the pI:C-treated F1 mice. NK cells have been demonstrated to be radioresistant; thus, as a test of our hypothesis, we examined the effects of irradiation on the capacity of pI:C treated F1 mice to reject B6 lymphocytes. The results show that this capacity was not blocked by 750 cGy, a dose of radiation that abrogates most T and B cell functions. Furthermore, rejection of parental cells could be prevented by treatment of recipient F1 mice with antibodies to asialo GM1, a treatment that suppresses NK activity. These data demonstrate that pI:C-mediated protection from GVH-induced changes is due to increased rejection of grafted B6 parental cells by F1 NK cells, a phenomenon very similar, if not identical, to HR to bone marrow grafts.     

GH3 cell secretion of growth hormone and prolactin increaseases spontaneously during perfifusion

Summary GH₃ cell secretory activity was studied in long-term perifusion to define previously reported spontaneous increases in growth hormone (GH) and prolactin production (PRL). Mechanically harvested cells (1×10⁷/column) were perifused at 4 ml/h for 72 h. A basal period of variable duration (8 to 12 h), during which hormone secretion was stable, was followed by steadily increasing secretion rates. Changes in cell number were not sufficient to acount for increased jormone secretion rates: a) there was no significant change in cell count after 72 h (0.97±0.03×10⁷;n=18); b) mean cell column DNA content increased 25.5% above the base value, whereas GH secretion rose 385% and PRL rose 178% (n=5). Observed differences in the duration of the basal secretion period, the basal secretory rate, and the magnitude of secretory rate increase were associated with several variables: a) variablility within a subline was a function of passage number: GH secretion decreased and PRL secretion increased with subculture number; b) cells with identical lot and freeze numbers, but received at different times, behaved differently; c) the presence of an antifungal agent (nystatin) altered hormone secretion reproducibly. Conclusions: a) rates of GH and PRL secretion rise spontaneously in perifusion without a proportional increase in GH₃ cell number; b) fluctuations in the rate of GH₃ cell secretion of GH and PRL are not entirely random but are determined by several definable variables. Supported by a grant to MES from the National Institutes of Health (AM33388) and in part by the Medical Research Service of the Veterans Administration.     

Reduction of T-kininogen messenger RNA levels by dexamethasone in the adjuvant-treated rat

When inflammation is induced in rats following injection of Freund's complete adjuvant, steady state levels of T-I and T-II kininogen mRNAs increase markedly as do plasma levels of T-I and T-II kininogens. When rats are additionally treated with dexamethasone, T-I and T-II steady state mRNA levels and plasma levels of T-kininogens are reduced. The results suggest that dexamethasone may affect the magnitude of T-kininogen gene induction caused by inflammation.     

Fibronectin turnover in human mesangial cell cultures as affected by Adriamycin

Fibronectin (FN) turnover and turnover changes induced by the anticancer drug Adriamycin (ADR) were measured in human mesangial cells (HMC) in vitro. HMC cultures synthesize cellular FN (2.2+-0.3% of totalprotein synthesis; n = 12) which is secreted and incorporated into a fibrillar extracellular matrix (ECM). A 24 hr incubation of HMC with ADR (0.5–5 g/ml) resulted in an accumulation of FN in the culture medium, with a maximum increase following 5 pglml(7.3+-2.3pg/cell vs. controls: 4.4+-1.9pg/cell; n= 10). Correspondingly, radioactively labeled immunoprecipitable FN was increased in a dosage-dependent manner in the culture medium up to 50% vs. controls. The incorporation of radioactively labeled FN into ECM was significantly increased following 2 g ADR/ml. In accordance, immunofZuorescence staining revealed an expansion ofpericellular FNfibers in cultures exposed to 2 g ADR/ml. Concomitant with the accumulation of extracelhlar FN, radioactively labeled FN in the cells was reduced by 22%. Qualitative characterization of FN patterns revealed a diminished number of degradation products in the culture medium ofADR-treated HMC. These data suggest thatADR interferes with the turnover of FN secreted by HMC in vitro in such a way that FN accumulates extracellularly. This in turn leads to a reduced FN synthesis. These findings are compatible with a loss of urinary FN degradation products accompanying the onset ofproteinuria in ADR-treated rats.Abbreviations ADR adriamycin - BSA bovine serum albumin - DTT dithiothreitol - ECM extracellular matrix - EDTA ethylenediamine tetraacetic acid disodium salt - ELISA enzyme-linked immunosorbent assay - FCS fetal calf serum - FITC fluorescein isothiocyanate - FN fibronectin - HMC human mesangial cell - PBS phosphate buffered saline - PMSF phenylmethylsulfonyl fluoride - SDS sodium dodecyl sulfate - SDS-PAGE SDS-polyacrylamide gel electrophoresis     

Solubilization and hydrophobicity test by Triton X-114-partitioning of NADPH-protochlorophyllide oxidoreductase from the unicellular alga Scenedesmus obliquus, mutant C-2A'

NADPH-protochlorophyllide oxidoreductase (PChilde reductase, EC 1.3.1.33), a key enzyme in light-dependent greening and the conversion of etioplasts into chloroplasts was investigated in the the greening mutant C-2A' of the unicellular green alga Scenedesmus obliquus. In the absence of detergent, the solubilization of the enzyme increased with high glycerol concentrations in the buffer. Solubilization capacities of 4 non-ionic or zwitterionic detergents, Triton X-100, CHAPS, octylglucoside and decyl-maltopyranoside, were compared. Due to the addition of these detergents, the enzyme activity in the soluble fraction was increased severalfold. Hydrophobicity of the enzyme was analyzed by Triton X-114 phase partitioning. The protein had a preference for the aqueous phase, but its distribution was strongly influenced by the glycerol concentration of the buffer. These results indicate that the PChlide reductase of the green alga Scenedesmus obliquus is a hydrophobic, membrane-associated enzyme, but not an integral membrane protein.