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Biomedical subjects

K Binder

Publications and source records attributed to K Binder.

At least 55 records · Page 3Linked to original sources

Calcidiol, calcitriol and parathyroid hormone serum concentrations in institutionalized and ambulatory elderly in Switzerland.

AIM: The aim of the present study was to measure concentrations of vitamin D metabolites and intact parathyroid hormone (iPTH) serum concentrations and an urinary bone resorption marker in two groups of elderly subjects, who differed markedly in their sedentary status and seasonality. DESIGN: 193 institutionalized elderly people of a long-stay geriatric ward (106 women: mean age 82; 87 men: mean age 78) were studied during wintertime. 312 ambulatory elderly people (109 women: mean age 74; 203 men: mean age 76) were studied during summertime. Concentrations of calcidiol (25(OH)D), calcitriol (1,25(OH)2D) and serum iPTH, as well as urinary N-telopeptides (NTX) were measured. RESULTS: Vitamin D deficiency (defined as serum 25(OH)D < 12 ng/ml) was present in 86% of institutionalized at the expected nadir (wintertime), compared to 15% of the ambulatory elderly subjects at the expected maximum (summertime). Serum calcitriol concentrations were significantly lower in institutionalized subjects (p = .0001). However intact PTH concentrations did not differ significantly between institutionalized and ambulatory elderly. Institutionalized and female subjects showed higher urinary NTX excretion (female institutionalized: 131.9; female ambulatory: 66.8/male institutionalized: 76.3 male ambulatory: 45.8 nmol/mmol). CONCLUSION: This cross-sectional study documented very low serum calcidiol and calcitriol concentrations and high urinary N-telopeptide excretion in institutionalized elderly people. There was no difference in serum iPTH concentrations between institutionalized and ambulatory elderly. This finding could not be explained by the differences in calcidiol and calcitriol concentration, nor urinary NTX excretion. These results suggest that other factors than vitamin D deficiency, such as lower mobility status and sedentary life style, might have an important role in the regulation of iPTH and mechanisms of bone loss in the elderly.

Aged↗

Elastic modulus of equine hoof horn, tested in wall samples, sole samples and frog samples at varying levels of moisture.

The elastic (E-) modulus of hoof horn samples as a function of moisture content was determined from different segments of the equine hoof. 110 hoof horn specimens with different pigmentation taken from six adult warm-blooded horses with no obvious pathological changes within t he foot were used for the 177 tension and bending tests which were performed in accordance with ASTM D 5026, ASTM D 5023 and DIN 53.457. E-moduli were determined under physiological conditions with mean 761.8, SD +/- 295.4 N/mm for dorsal wall samples, 708 +/- 280.4 N/mm2 for lateral wall samples, 230 +/- 92.4 N/mm2 for sole horn and 9.9 +/- 0.6 N/mm2 for frog horn. Dorsal wall and lateral wall did not differ significantly. E-moduli of the various hoof horn segments differ significantly when tested under physiological moisture. The physiological moisture content also varies significantly between the segments: wall samples mean 22.7 +/- SD 3.4%, sole samples 31.5 +/- 3.1%, frog samples 34.6 +/- 3.3%. In contrast, the E-moduli and the moisture contents of the various segments were approximately identical, when tested after drying at 65% humidity over 6 days.

Animals↗

Hepatic ultrasonographic findings in experimental carbon tetrachloride intoxication of the dog.

An experimental study was undertaken in dogs with carbon tetrachloride (CCl4) intoxication to describe and follow the changes in the ultrasound appearance of the liver. Characteristic ultrasound features (enlarged liver, increased echogenicity with fine, tightly-packed echoes, and loss of echogenicity of the portal vein walls) were seen from day 2 of the experiment, culminating between days 2 and 7. Subsequently the liver gradually and almost completely regained its normal ultrasound appearance. Ultrasonographic findings corresponded to the severity of the clinicopathological parameters, and changed parallel with the results of liver biopsies. Histology of the biopsy samples revealed acute centrolobular lipid accumulation with necrobiosis and necrosis in the hepatocytes in the first stage of the disease. In the second stage, a secondary reparatory-inflammatory process and reparation in the interstitial tissue were seen. In some dogs, ill-defined hyperechoic foci were observed within the liver during the regenerative phase. Hepatic ultrasonography seems to be a reliable and relatively sensitive method for monitoring liver dystrophy with necrobiosis and lipid accumulation and to follow the course of steatosis in clinical cases. Ultrasound-guided biopsy can further improve the diagnostic accuracy of ultrasonography in liver dystrophy.

Alanine Transaminase↗

Inhibition of minK protein induced K+ channels in Xenopus oocytes by estrogens.

Previously it was shown that minK protein expression in uterus is regulated by estrogen. In the present study, we were interested in putative direct effects of estrogen on minK protein induced K+ currents (IminK) in Xenopus oocytes. Superfusion with 17-beta-estradiol (1 microM) resulted in an inhibition of minK-induced currents, but had no appreciable effects on the delayed rectifier and inward rectifier K+ channels Kv1.1 and Kir2.1, respectively. The inhibition of IminK by 17-beta-estradiol was concentration-dependent, with an IC50 of approximately 0.5 microM. In the presence of 17-beta-estradiol, the conductance-voltage relationship was shifted to more depolarized potentials. IminK inhibition occurred also in the presence of the estrogen-receptor antagonist tamoxifen, suggesting that a mechanism independent of estrogen receptors is involved. The synthetic estrogen diethylstilbestrol (DES) also inhibited IminK but with a lower affinity (IC50 of 4.5 microM), while cortisol and progesterone had only weak effects on IminK. In summary, the results indicate that estrogens directly inhibit IminK.

Animals↗

Both tumor necrosis factor receptors, TNFR60 and TNFR80, are involved in signaling endothelial tissue factor expression by juxtacrine tumor necrosis factor alpha.

We have investigated the role of the two distinct tumor necrosis factor (TNF) receptors (TNFR60 and TNFR80) in endothelial cell activation employing an in vitro model of tumor necrosis factor alpha (TNF-alpha)-dependent tissue factor production of human umbilical vein endothelial cells (HUVECs). In this model, tissue factor is produced either on addition of exogeneous TNF-alpha, or by induction of endogenous TNF-alpha via adhesion molecule-linked signal pathways. Under both conditions, tissue factor expression could be partially blocked by antagonistic antibodies against either TNFR60 or TNFR80 and was fully inhibited by simultaneous application of both antibodies. Selective inhibitors of either TNFR60 or TNFR80-induced signal pathways inhibited tissue factor expression, and selective triggering of either of the two TNF receptors by agonistic antibodies induced this response in HUVECs. Furthermore, a coculture system of HUVECs and Chinese hamster ovary transfectants expressing a noncleavable, exclusively membrane-bound form of TNF-alpha resulted in a potent activation of HUVECs with synergistic action of both TNF receptors. Together, these data underline the importance of juxtacrine pathways in endothelial cell activation of procoagulant functions and show that membrane TNF-alpha and both TNFR types play a critical role.

Cell Adhesion Molecules↗

Signaling by E-selectin and ICAM-1 induces endothelial tissue factor production via autocrine secretion of platelet-activating factor and tumor necrosis factor alpha.

Based on previous studies showed adhesion molecule-dependent induction of tissue factor upon endothelium-lymphocyte interactions, we investigated whether E-selectin and ICAM-1 are linked to signaling pathways leading to tissue factor gene expression. Cellular interaction was mimicked by antibody cross-linking of E-selectin and ICAM-1 on the surface of human umbilical vein endothelial cells (HUVECs), resulting in induction of tissue factor mRNA and protein expression. Tissue factor production could be independently abolished by antibodies against TNF-alpha and by WEB 2086, a platelet-activating factor (PAF) receptor antagonist. Because WEB 2086 prevented the production and/or secretion of TNF-alpha by HUVECs, these results provide evidence for E-selectin- and ICAM-1-linked signal pathways leading to tissue factor synthesis in endothelial cells via an autocrine feedback loop involving PAF and TNF-alpha secretion.

Antigen-Antibody Reactions↗