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Insulin regulation of amino acid transport in mesenchymal cells from avian and mammalian tissues.
Insulin regulation of amino acid transport across the cell membrane was studied in a variety of mesenchymal cell directly isolated from avian and mammalian tissues or collected from confluent cultures. Transport activity of the principal systems of mediation in the presence and absence of insulin was evaluated by measuring the uptake of representative amino acids under conditions approaching initial entry rates. Insulin enhanced the transport rate of substrate amino acids from the A system(alpha-aminoisobutyric acid, L-proline, glycine, L-alanine and L-serine) in fibroblasts and osteoblasts from chick-embryo tissues, in mesenchymal cells (fibroblasts and smooth muscle cells) from immature rat uterus, in thymic lymphocytes from young rats and in chick-embryo fibroblasts from confluent secondary cultures. In these tissues, the uptake of amino acid substrates of transport systems L and Ly+ (L-leucine, L-phenylalanine, L-lysine) was not affected by the presence of the hormone. No insulin control of amino acid transport was detected in chick-embryo chondroblasts and rat peritoneal macrophages. These observations identify the occurrence of hormonal regulatory patterns of amino acid transport for different mesenchymal cells types and indicate that these properties emerge early during cell differentiation
ZOLEDRONIC ACID DETERMINES S-PHASE ARREST BUT FAILS TO INDUCE APOPTOSIS IN CHOLANGIOCARCINOMA
Heat shock proteins and the cellular response to osmotic stress
In antidiuresis, the intrarenal distribution of HSP25/27, alpha beta -crystallin, HSP72, OSP94 and HSP110 corresponds to the osmotic gradient between cortex and papilla: low amounts in the cortex and high values in the inner medulla and papilla. In addition, medullary HSP72 levels change appropriately with the diuretic state. Studies on MUCK cells suggest that, in the renal medulla in vivo, stressors, such as NaCl and low pH, may act in concert to induce HSP72 expression. Urea, added to the medium at high concentrations (600 mM), causes the majority of MUCK cells to die. Prior exposure of these cells to hypertonic media (NaCl addition), a maneuver that induces HSP72, protects the cells against the deleterious effects of high urea concentrations. Inhibition of HSP72 expression by stable antisense transfection or SB203580 treatment abolishes the beneficial effects of prior hypertonic stress. Conversely, overexpression of HSP72 under isotonic conditions by a dexamethasone-driven vector confers substantial resistance against subsequent exposure to high urea concentrations. Taken together these results suggest that also in the renal inner medulla, NaCl-induced enhancement of HSP72 expression may help counteract the detrimental effects of high urea concentrations. Copyright (C) 2000 S. Karger AG Basel
Methodology for the assessment of lung protection. Human pulmonary artery endothelial cell preservation using haemaccel.
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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