Hot erosion wear and carburization in petrochemical furnaces

High temperature alloy stainless steels used in olefins manufacturing furnaces are exposed to extreme environmental degradation processes inclusive of carburization, oxidation and hot erosion wear. A study was undertaken to understand the hot erosion wear phenomenon in relation to substrate composition, atmosphere, temperature, time and the influence of carburization. An erosion wear test rig was designed and constructed to simulate the wear degradation process up to 1200°C. Results have shown a surprising relationship between erosion wear rate and temperature for the most prominent stainless steel alloy used in the industry. A novel coating technology was developed for mitigation that enables the non‐line‐of‐sight application of protective macro‐coatings typically 1 to 5 mm in thickness. Stainless steel coupons treated with these macro‐coatings have exhibited an enhanced resistance to both oxidation and carburization. These macro‐coatings also provide superior hot erosion wear resistance as compared to the uncoated stainless steel. A thorough examination of the microstructure and micro‐mechanical properties of the coatings is presented. Targeted applications include petrochemical furnace fittings (return bends), thermo‐wells and transfer‐line‐exchanger (TLE) surfaces. Commercial furnace trials of the prototype products have been initiated with some prototypes in field trials for over 18 months. Results of both laboratory accelerated testing and field evaluation will be discussed.     

Interleukin-1 beta increases leukemia inhibitory factor mRNA levels through transient stimulation of transcription rate

The aim of this study was to determine immunogenetic markers of susceptibility in Crohn's disease (CD), taking the different features of the clinical course of the disease into account. HLA class I, HLA class II and TAP transporter gene polymorphisms were studied using DNA typing methods. Gene and antigen frequencies were analysed and compared in a group of 102 CD patients and 200 unrelated healthy controls from the same area. Analysis of the whole CD patient population revealed no definite association with either HLA or TAP gene alleles, with the exception of an association with DRB1*1302 (Pc < 0.05). However, when clinical subgroups of patients were considered, specific associations with some genetic markers were found. The most definitive results involved a genetic association in the group of patients who did not respond to glucocorticoid therapy. This group was characterized by a high frequency of HLA-DRB1*04 (P < 0.05). Conversely, a positive association with the TAP2-A allele was found in cortico-responder patients (Pc < 0.03). Furthermore, analysis of the distribution of HLA class II alleles in relation to the presence of extra-intestinal manifestations revealed an association with the DQB1*0501 or *0503 suballele of DQ5 (P < 0.05). Finally, patients with lesions in the small bowel were more frequently HLA DRB1*07 (P < 0.05). The present study supports the concept of clinical heterogeneity in Crohn's disease associated with a background of genetic heterogeneity.     

ICAM-1 upregulation in distant tissues after hepatic ischemia/reperfusion: a clue to the mechanism of multiple organ failure

BACKGROUND/PURPOSE: Endothelial cell adhesion molecules (ECAMs) are felt to play an important role in ischemia/reperfusion (I/R) injury by causing adhesion of leukocytes to endothelial cells. It is possible that ECAMs play a role in multiple organ system failure. ICAM-1 is one of the adhesion molecules that has been shown to be upregulated in response to cytokines. This upregulation leads to leukocyte endothelial cell interaction (adhesion) and to neutrophil infiltration of the affected tissue. The purpose of our study was to measure ICAM-1 expression in the liver and other organs after hepatic ischemia/reperfusion (I/R). METHODS: A laparotomy was performed on 14 Sprague-Dawley rats; 45 minutes of occlusive ischemia to the left lateral lobe was followed by 5 hours of reperfusion. The rat was injected with I125-labeled ICAM-1 MAb and I131-labeled nonbinding MAb (to control for nonspecific accumulation of ICAM-1 MAb). Entire organs were harvested and accumulated activity was measured in each organ. ICAM-1 levels were expressed as percent injected dose per gram of tissue. Control animals underwent sham laparotomy. RESULTS: ICAM-1 was upregulated in the ischemic lobe of the liver, nonischemic lobe of the liver, heart, kidney, intestine, and pancreas. Up-regulation in the lung was not significant. Both the lung and liver had high constitutive levels of ICAM-1. CONCLUSIONS: These data show that (1) significant hepatic upregulation of ICAM-1 after hepatic ischemia/reperfusion and (2) significant ICAM-1 upregulation in other tissues (heart, kidney, and intestine) after hepatic ischemia/reperfusion. The ICAM-1 upregulation in distant organs is likely mediated by cytokines such as tumor necrosis factor (TNF). These data show that leukocyte endothelial cell interactions in distant organs may be mediated by hepatic ischemia/reperfusion. This is a possible explanation for how failure of one organ can lead to failure of others in multiple organ system failure.     

General practitioner funding policy: from where to whither?

Six public policy objectives relating to general practitioner (GP) funding since 1938 have been identified. They concern national health insurance, rural GP shortages, care for the poor, health promotion, cost effectiveness and community control. Each of these objectives is examined in turn, focusing on the extent to which each has been met. In all cases past policies have been, at best, only partially successful in meeting their objectives and have required little in the way of dismantling prior to the introduction of new GP funding initiatives subsequent to 1993. Theoretical principles relating to the development of efficient and coherent public policy are discussed. New Zealand policy relating to funding of GP services has rarely conformed to such principles. There is an emerging consensus between social democrats and libertarians that targeted programmes for the poor is the equitable and efficient way to proceed. A key policy decision concerns the balance between planned primary care services for low income groups and more traditional market style arrangements for others.     

Oxidant--nitric oxide signalling mechanisms in vascular tissue

Nitric oxide has several signalling mechanisms that can potentially control force generation by vascular smooth muscle. Some of these mechanisms include the stimulation of cGMP production by the soluble heme-containing form of guanylate cyclase (sGC), inhibition of mitochondrial respiration, and the modulation of vasoactive mediator release by the endothelium. Reactive O2 species (ROS) can also regulate force generation by vascular smooth muscle through mechanisms including the stimulation of production of vasoactive prostaglandins, the stimulation of sGC by catalase-mediated metabolism of H2O2 and inhibition of sGC activation by superoxide, the activation of protein kinase C, and the modulation of mediator release from the endothelium. Interactions between NO and ROS signalling mechanisms result in additional processes which modulate vascular force generation. For example, NO-elicited stimulation of sGC can be attenuated by superoxide, and this results in the formation of peroxynitrite (ONOO-). However, high levels of NO result in a ONOO- and thiol dependent formation of a species which regenerates NO in a time-dependent manner. It appears that NO inhibits catalase through an O2 and superoxide dependent process which results in inhibition of relaxation mediated by H2O2-elicited stimulation of sGC. Furthermore, evidence exists suggesting additional signalling mechanisms resulting from interactions between regulatory systems involving NO and ROS which appear to be important in control of vascular force generation in pathophysiological states.     

Activation of natural killer cells in arthritis-susceptible but not arthritis-resistant mouse strains following Borrelia burgdorferi infection

Infection of susceptible mouse strains with Borrelia burgdorferi, the agent of Lyme disease, results in the development of arthritis. Components of the innate immune system may be important mediators of this pathology. To investigate the potential role of NK cells in development of experimental Lyme arthritis, we examined their activation in vivo in both resistant and susceptible mouse strains. Following inoculation of B. burgdorferi into the footpad, lymph node NK cells from susceptible C3H/HeJ (C3H) mice produced more gamma interferon than NK cells from resistant DBA/2J mice. Lymph node cells from susceptible C3H and AKR mice also had increased ability to lyse YAC-1 target cells 2 days following infection. Antibody depletion of NK cells from susceptible mice, however, did not alter the development of arthritis following B. burgdorferi challenge. In addition, NK cell depletion had little effect on spirochete burden. Thus, there is a marked activation of NK cells in susceptible mouse strains following infection. Although NK cells are not absolutely required for arthritis, events occurring prior to NK cell activation might be important in mediating pathology in experimental Lyme disease.     

Familial hypoparathyroidism: identification of a novel gain of function mutation in transmembrane domain 5 of the calcium-sensing receptor

Activating mutations of the extracellular calcium (Ca2+e)-sensing receptor (CaR) gene, mostly in its extracellular domain, can cause both familial and sporadic hypoparathyroidism. We report a Japanese family with severe hypoparathyroidism with pretreatment serum calcium (Ca) levels of 4.9-5.9 mg/dL. The proband presented with a seizure at 6 days of age. Her older brother and mother, who had also experienced seizures and tetany, respectively, likewise had hypoparathyroidism. A heterozygous missense mutation substituting a cysteine for the phenylalanine normally present at codon 788 (F788C) was identified in the CaR's fifth transmembrane domain and was shown to cosegregate with the disease. The mutation was absent in DNA from 50 control subjects. Analysis of the functional properties of the mutant receptor was carried out in transiently transfected HEK293 cells loaded with fura-2 by assessing Ca2+e-evoked increases in the cytosolic calcium concentration (Ca2+i). There was a leftward shift in the concentration-response curve for the mutant receptor [EC50 (effective concentration of Ca2+e producing half of the maximal Ca2+i response, 2.7 +/- 0.1 vs. 4.1 +/- 0.1 mmol/L for the wild-type receptor]. HEK293 cells cotransfected with both the wild-type and mutant CaRs (to mimic the heterozygous state in affected family members) showed an EC50 (3.0 +/- 0.1 mmol/L) similar to that of the mutant CaR alone. Thus, we confirm that 1) a gain of function mutation in the fifth transmembrane domain of the CaR causes severe familial hypoparathyroidism by rendering the receptor more sensitive than normal to activation by Ca2+e; 2) some patients in the family do not experience seizures despite their severe hypocalcemia; and 3) this condition needs to be differentiated from other causes of hypoparathyroidism.     

Pathogenesis of wild-type and leaderless foot-and-mouth disease virus in cattle

Four calves were experimentally infected via aerosol with foot-and-mouth disease virus. Two were infected with a wild-type virus derived from a full-length infectious clone (A12-IC), and two were infected with a clone-derived virus lacking the leader gene (A12-LLV2), with euthanasia and tissue collection at 24 and 72 h postexposure (hpe). Clinical disease was apparent only in the animal given A12-IC and euthanized at 72 hpe. In situ hybridization revealed that the animal infected with A12-IC and euthanized at 24 hpe had abundant viral nucleic acid in the lung, present in clusters of positive cells in the respiratory bronchiolar epithelium and associated subepithelial regions. At 72 hpe in the A12-IC-infected calf, viral nucleic acid in the lung was present in interstitial areas, and in addition, viral nucleic acid was detectable in epithelial tissues around histologically apparent vesicles. In animals infected with A12-LLV2, viral nucleic acid was detectable in the lung at both 24 and 72 hpe, but staining revealed a more localized distribution with less nucleic acid than was found in animals given A12-IC. Therefore, it appears that after aerosol exposure to A12-IC, early replication is in the region of the lung, with subsequent dissemination to distal sites. In comparison, the A12-LLV2 virus is much less widely disseminated in the lung at 24 hpe, with no lesions or virus detectable in secondary sites at 72 hpe. The greatly reduced pathogenicity of A12-LLV2 may make it an excellent candidate for a modified live viral vaccine.     

Transitioning to independence: challenges for young people with disabilities and their caregivers

For all teens, the process of moving from childhood to adulthood is challenging. For young people with disabilities, transitioning to independence presents even more challenges. Barriers to successful transition for young people with disabilities include low expectations by parents and other significant people in the community, lack of knowledge of existing career and vocational education services, and lack of self-advocacy skills. This article provides an overview of issues related to transitioning to adult independence and offers suggestions for assessment, planning, and intervention that can help nurses be effective partners with families and other caregivers in transition efforts. Nurses caring for children with disabilities can help families see strengths in their children and develop realistic, developmentally-appropriate expectations for skill development, attitudes, and behaviors that will promote self-sufficiency in adulthood. Nurses can help families think about possibilities for independence and refer families to community resources that can help young people with disabilities pursue postsecondary education, obtain and maintain jobs, and live independently.     

Effects of flow on the fish communities of a regulated California river: implications for managing native fishes

We assessed the importance of flow regime to the success of native and non‐native fish species by analysing winter/spring seining data collected from 1987 to 1997 on the resident fish communities of the lower Tuolumne River, California. The data were analysed using regression models to predict the percentage of non‐native fish at a site. The regression models included various combinations of the variables longitudinal location of the site, mean April/May stream discharge in the year of sampling, and mean April/May stream discharge in the previous year. Comparison of the models indicated that the best model included longitudinal location and stream discharge in the previous year. This model is consistent with the hypothesis that flow in the previous year differentially affects reproductive success of native and non‐native species and thus the resulting community sampled in the following winter/spring. A detrended correspondence analysis of percentage abundance species data identified a co‐occurring group of native species and a co‐occurring group of non‐native species with the non‐native red shiner (Cyprinella lutrensis) grouping separately. The differing reproductive strategies of the species were consistent with the hypothesis concerning spawning success. Our results indicate that flow regime is an important determinant of the reproductive success of native and non‐native fish species in regulated rivers. Manipulations of flow regime are a potentially powerful tool for managing native fish species, but should be considered in combination with other restoration efforts and in the context of ecosystem restoration. Copyright © 2002 John Wiley & Sons, Ltd.