Overexpression of human superoxide dismutase inhibits oxidation of low-density lipoprotein by endothelial cells

Oxidation of LDL in the subendothelial space has been proposed to play a key role in atherosclerosis. Endothelial cells produce superoxide anions (O2.-) and oxidize LDL in vitro; however, the role of O2.- in endothelial cell-induced LDL oxidation is unclear. Incubation of human LDL (200 microg/mL) with bovine aortic endothelial cells (BAECs) for 18 hours resulted in a 4-fold increase in LDL oxidation compared with cell-free incubation (22.5+/-1.1 versus 6.3+/-0.2 [mean+/-SEM] nmol malondialdehyde/mg LDL protein, respectively; P<0.05). Under similar conditions, incubation of LDL with porcine aortic endothelial cells resulted in a 5-fold increase in LDL oxidation. Inclusion of exogenous copper/zinc superoxide dismutase (Cu/ZnSOD, 100 microg/mL) in the medium reduced BAEC-induced LDL oxidation by 79%. To determine whether the intracellular SOD content can have a similar protective effect, BAECs were infected with adenoviral vectors containing cDNA for human Cu/ZnSOD (AdCu/ZnSOD) or manganese SOD (AdMnSOD). Adenoviral infection increased the content and activity of either Cu/ZnSOD or MnSOD in the cells and reduced cellular O2.- release by two thirds. When cells infected with AdCu/ZnSOD or AdMnSOD were incubated with LDL, formation of malondialdehyde was decreased by 77% and 32%, respectively. Two other indices of LDL oxidation, formation of conjugated dienes and increased LDL electrophoretic mobility, were similarly reduced by SOD transduction. These data suggest that production of O2.- contributes to endothelial cell-induced oxidation of LDL in vitro. Furthermore, adenovirus-mediated transfer of cDNA for human SOD, particularly Cu/ZnSOD, effectively reduces oxidation of LDL by endothelial cells.     

Identification and characterization of novel substrates of Trk receptors in developing neurons

Neurotrophins influence growth and survival of specific populations of neurons through activation of Trks, members of the receptor tyrosine kinase (RTK) family. In this report, we describe the identification and characterization of two substrates of Trk kinases, rAPS and SH2-B, which are closely related Src homolog 2 (SH2) domain-containing signaling molecules. rAPS and SH2-B are substrates of TrkB and TrkC in cortical neurons and SH2-B is a substrate of TrkA in sympathetic neurons. Moreover, rAPS and SH2-B bind to Grb2, and both are sufficient to mediate NGF induction of Ras, MAP kinase (MAPK), and morphological differentiation of PC12 cells. Lastly, antibody perturbation and transient transfection experiments indicate that SH2-B, or a closely related molecule, is necessary for NGF-dependent signaling in neonatal sympathetic neurons. Together, these observations indicate that rAPS and SH2-B mediate Trk signaling in developing neurons.     

Diagnosis of hyperventilation for elimination of false-positive results of physical exercise test

The study was conducted in 55 patients with cardiac pains. Electrocardiography was used successively prior to, during and following physical exercises, followed by Seldinger selective coronary angiography, and electrocardiography prior to, during and following hyperventilation tests. In 2 of 55 patients the result of the exercise test was interpreted as false-positive, since the coronary angiography demonstrated intact vessels, and during hyperventilation ECG recorded a decreased ST segment. To avoid false-positive results in patients with suspected angina pectoris the physical exercises tests can be considered positive only in cases in which hyperventilation caused no ECG changes typical for angina pectoris.     

Effects of cognitively induced anxiety on hand temperature

This study explored the relationship of cognitively induced anxiety and hand temperature reduction in a nonclinical sample. Forty college students were randomly assigned to either the Anxiety Group or the Pleasant Group. Following a baseline period, individuals in the Anxiety Group discussed with the experimenter topics which were anxiety-producing for them. Individuals in the Pleasant Group discussed topics of a pleasant nature. During these discussions, hand temperatures were recorded from the palmar surface of the third finger on the dominant hand. Data analysis indicated that hand temperature decreases were significant only in subjects discussing anxiety-producing topics.     

Binding of an arm repeat protein to the kinase domain of the S-locus receptor kinase

Screening of a yeast two-hybrid library for proteins that interact with the kinase domain of an S-locus receptor kinase (SRK) resulted in the isolation of a plant protein called ARC1 (Arm Repeat Containing). This interaction was mediated by the C-terminal region of ARC1 in which five arm repeat units were identified. Using the yeast two-hybrid system and in vitro binding assays, ARC1 was found to interact specifically with the kinase domains from SRK-910 and SRK-A14 but failed to interact with kinase domains from two different Arabidopsis receptor-like kinases. In addition, treatment with a protein phosphatase or the use of a kinase-inactive mutant reduced or abolished the binding of ARC1 to the SRK-910 kinase domain, indicating that the interaction was phosphorylation dependent. Lastly, RNA blot analysis revealed that the expression of ARC1 is restricted to the stigma, the site of the self-incompatibility response.     

Changes in the ultra-fine structure of capillaries of the embryonic brain in the presence of schizophrenia in the mother

The report is concerned with a study of fine structures of brain capillaries in 9 embryos received during medical abortions from schizophrenic mothers. The authors established some traits in the ultrastructure of endothelial cells in most of the studied cases--an increase of the surface of endothelial cells at the expense of a tortuosity of their plasmatic membranes and a formation of growths, vacuolization of the cytoplasma. There were also some changes in the structure of basal membranes. In 2 cases there were also peculiar pathological changes in the vascular endothelium: granules of an unknown nature in the endothelial cells and a focal lysis of the plasmatic membranes of endothelial cells.