Role of Error-Recovery Process in Projects

To reduce errors in projects, knowledge about their causes, through examining their chain of events, and costs should be made available. With this in mind, this paper examines the role of the error recovery process in detecting human-related errors with reference to seven Swedish building construction projects. A total of 2,879 human errors were identified, and those that were found to be the most costly were examined in detail. Industry practitioners’ opinions as to how the identified errors could have been prevented were solicited. It was revealed that the major areas of error reduction lay with improving communication between participants, introducing incentives, improving resourcing levels in projects particularly during design, and the encouragement of individual and organizational learning. The paper concludes by suggesting that the most effective learning takes place in projects when the entire error-recovery process is performed (i.e., detection, indication, and correction) and not parts thereof.     

Breast cancer screening in Navarra: interpretation of a high detection rate at the first screening round and a low rate at the second round

Endothelial cells and pericytes are closely associated in brain capillaries. Together with astrocytic foot processes, they form the blood-brain barrier. Capillaries were isolated from bovine brain cortex. Pure populations of endothelial cells and pericytes were isolated and cultured in vitro. Polarized monolayers of endothelial cells preferentially secreted immunoreactive endothelin-1 (Et-1) at their abluminal (brain-facing) membrane. They did not express receptors for Et-1. Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments. These receptors were coupled to phospholipase C as demonstrated by intracellular calcium measurements using indo-1-loaded cells. Addition of Et-1 to pericytes induced marked changes in the cell morphology that were associated with a reorganization of F-actin and intermediate filaments. It is concluded that Et-1 is a paracrine mediator at the bovine blood-brain barrier and that capillary pericytes are target cells for endothelium-derived Et-1.     

Reactive oxygen intermediates mediate a systemic signal network in the establishment of plant immunity

Recognition of an avirulent pathogen stimulates an oxidative burst generating O2- and H2O2, and these reactive oxygen intermediates (ROIs) cue the induction of defense genes and cell death in the development of a restricted lesion. This localized hypersensitive response (HR) is accompanied by the development of systemic acquired resistance to virulent pathogens. Here we show that inoculation of Arabidopsis leaves with avirulent Pseudomonas syringae induces secondary oxidative bursts in discrete cells in distant tissues, leading to low-frequency systemic micro-HRs. The primary oxidative burst induces these systemic responses, and both the primary burst and the secondary microbursts are required for systemic immunity. Hence, ROIs mediate a reiterative signal network underlying systemic as well as local resistance responses.     

Electrical basis of peristalsis in the mammalian upper urinary tract

1. Peristalsis in the mammalian upper urinary tract (UUT) is mostly myogenic in origin, originating predominately in the proximal pelvicalyceal regions of the renal pelvis, an area that is enriched with specialized smooth muscle cells termed 'atypical' smooth muscle cells. Propagating peristaltic contractions are little affected by blockers of either autonomic nerve function or nerve impulse propagation; however, blockers of sensory nerve function or prostaglandin synthesis reduce both the frequency and the strength of the spontaneous contractions underlying peristalsis. 2. The electrical drive for these peristaltic contractions has long been considered to involve mechanisms analogous to the heart, such that 'atypical' smooth muscle cells generate spontaneous 'pacemaker' action potentials. These pacemaker potentials trigger the firing of action potentials and contraction in the muscular regions of the renal pelvis, which propagate distally to the ureter, propelling urine towards the bladder. 3. Recent intracellular microelectrode and single cell/channel patch-clamp studies have revealed that the ionic conductances underlying the action potentials recorded in the UUT are likely to involve the opening and slow closure of voltage-activated 'L-type' Ca2+ channels, offset by the time-dependent opening and closure of both voltage- and Ca(2+)-activated K+ channels. 4. In the present review we summarize the current knowledge of the ionic mechanisms underlying action potential discharge in the UUT, as well as present our view on how this electrical activity supports the initiation and conduction of UUT peristalsis.     

Anphen and energy status of the animal body

Energy status of rats was altered after administration of anphen [2,4-(hydroxy-3,5-ditretbutyl phenyl)-2-aminomalonic acid] at a dose of 40 mg/kg. Within 30 min after administration, maximal rates of NAD-dependent substrates and succinate oxidation were detected in liver mitochondria, which appears to occur due to activation of the mitochondrogenesis. The rate of electron transport in respiratory chain of mitochondria was decreased 1.3-1.6-fold within 1-1.5 hr, whereas within 3 hrs the patterns of oxidation and energetic coupling in liver mitochondria were reduced to control values. The similar alterations were observed in activities of lymphocyte alpha-glycerophosphate- and succinate dehydrogenases. Shifts in the pool of lipid peroxidation products in biological membranes was apparently responsible for alterations in activity of the energy metabolizing enzymes in lymphocytes and liver mitochondria.     

Opposing effects on modulation of angiogenesis by protein kinase C and cAMP-mediated pathways

The role of cAMP-mediated pathway in modulating angiogenesis was investigated. We have shown previously that activators of protein kinase C (PKC) caused a marked increase in angiogenesis, while the specific inhibitor of PKC, Ro 318220 suppressed angiogenesis. Here we show that forskolin, which activates adenylate cyclase and elevates the intracellular levels of cAMP, and the Sp-diastereomer of adenosine cyclic-3',5'-monophosphothioate (Sp-cAMPS), caused a dose-dependent suppression of collagenous protein biosynthesis and angiogenesis in the chick chorioallantoic membrane system (CAM). The opposite modulation of angiogenesis by activators of PKC and elevated cAMP levels was further confirmed by the suppression of 4 beta-phorbol-12-myristate-13-acetate (4 beta-PMA)-stimulated angiogenesis by either forskolin or Sp-cAMPS. On the contrary, the Rp-diastereomer of adenosine cyclic-3',5'-monophosphothioate (Rp-cAMPS), which antagonises endogenous cAMP biochemical actions, had no effect on angiogenesis alone and did not suppress 4 beta-PMA stimulated angiogenesis. However, Rp-cAMPS antagonised the effect of forskolin and Sp-cAMPS on 4 beta-PMA induced angiogenesis. Similar results were obtained in the human umbilical vein endothelial cell tube formation assay. In this system, the PKC inhibitor, Ro 318220, caused a dose-dependent inhibition of 4 beta-PMA reversed this effect. Also, forskolin and Sp-cAMPS caused an inhibition in tube formation. These results indicate that increased levels of intracellular cAMP have a negative effect in normal angiogenesis and cause a large reduction of the promotion of angiogenesis resulting from PKC activation.